ElShamah - Reason & Science: Defending ID and the Christian Worldview
Would you like to react to this message? Create an account in a few clicks or log in to continue.
ElShamah - Reason & Science: Defending ID and the Christian Worldview

Otangelo Grasso: This is my personal virtual library, where i collect information, which leads in my view to the Christian faith, creationism, and Intelligent Design as the best explanation of the origin of the physical Universe, life, biodiversity


You are not connected. Please login or register

Chimps, our brothers ?

Go down  Message [Page 1 of 1]

1Chimps, our brothers ?  Empty Chimps, our brothers ? Sat Jan 16, 2016 11:32 pm

Otangelo


Admin

Chimps, our brothers ? 

https://reasonandscience.catsboard.com/t2272-chimps-our-brothers

from Marcos Eberlins excellent book: 
Life and the Universe by Intelligent Design

https://www.widbook.com/ebook/read/life-and-the-universe-by-intelligent-design


Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Sem_ty23


Figure 2. Branch of "legendary Tree of Life" which "illustrates" best monkey-homo sapiens evolution from the "primal hominid", the one of Dryopithecus. Is it?
Could it be that this whole story is based on facts, or are they just rumors? Then we go to them, to the facts, and ten of them, and see which of them can be concluded:
1. fossil record. Is the monkey-man evolution there documented in the fossil record - the "Museum of Life"? As we have discussed in this book, in Chapter 48, it has passed more than 150 years of serious and intensive paleontological investigation. And that scour today shows an abundant fossil record and well established, and many monkeys fossil specimens - chimpanzees, gorillas and orangutans - and humans. But how are these fossils of apes and men? The answer is clear and unequivocal: the fossils are very, very similar to apes and men we know today, and vary as the same range today. They are numerous fossils of man and ape the "way" that apes and men are today well diversified, but there in the fossil record man is man and monkey is monkey. Ie King Kong King Kong, Tarzan is Tarzan, Jane is Jane, and Chita Chita is (Figure 3).

Chimps, our brothers ?  Sem_ty20
Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC

Figure 3. Tarzan, Jane and Cheetah: In the fossil record and in Hollywood, identical.
But then where are the "missing links" of transition? Where were the various links of the evolution of icons like those in Figure 2 - connecting apes and modern humans with our common ancestor ape - the Dryopithecus? Or was this a 'tabajaropithecus "? There were a number of alleged "missing links" like Lucy, as Java Man, and the Piltdown. What's more, Homo Erectus and Neanderthal man, and the latest soon to join these, Homo Nadeli. But they all, without exception, proved over time and further investigation as a farce or a big mistake. Or are even fossils of a man, or even a monkey. Ie, where inhabit these missing links ape-man? Where are they  found? The answer of this "where" is again vexatious for  "evolution": you will find such "missing links" only on the web, Google, blogs and fertile imagination of materialized evolutionary biologists - shamelessly - in biology textbooks via caricatures of evolution as that of Figures 1 and 2 

Darwin once said: "The amount of intermediate species should be huge, and the fossil record should be full of them, and this is perhaps the most serious and most obvious objection to my theory" 1 Darwin was right because the lack of intermediate species was - and still is, and it indicates that it will keep being - the most serious objection to Darwinian theory After 150 years, the shameful absence of transitional forms in the fossil record seems to annihilate Darwin's theory completely.The total, broad and unrestricted absence of intermediate species, not just monkey-man, but rat-bat, the "dino-bird", fish mammal, and many others, or rather literally all there in the fossil record - the "Museum of Life "- wide open for those who have eyes and want to see, seems to leave no doubt of the failure of a theory that once revolutionized the world.
2. Haldane and biochemistry mathematics . Haldane was a famous British geneticist, atheist and evolutionist. Note here that since he is a geneticist, academic  fellows, authors manifests will not be able to rotulate Haldane a "professional from other fields of knowledge." And for being a atheist and evolutionist, they can not classify him as a "pseudoscientist," but i can imagine they will try. Haldane became famous for developing a deadly dilemma for evolution, as calculated it would take 300,000 generations to fix a favorable mutation in a population.1 Several criticisms have been made against his calculations, but the "Haldane's Dilemma" has remained firm and strong.2,3  In 6 million years then, according to the calculations of Haldane, since supposedly the man separated from their "cousins", monkeys, only about 1,000 or about 2.000 3 of these mutations would have been fixed. But - we now know - we are about 33% genetically different from chimps.4 That is, with a 3.2 billion "bits" in the genome, we have nearly 1 billion different bits. Even using those estimates, "conservative" 3%, would still be at least 100 million.5 That is, the "wonder trio" of evolution simply had no time, even at 6 million years - because they are "slow" too - to change almost nothing in US. But we would have changed, and, 100-1000 times more than we could, according to evolution. So how do we change? Well, the calculations of Haldane were made for changes of "good" mutations, but we know today that deleterious mutations - the "evil" ones- are accumulated in us at an alarming rate, in what was called the genetic entropy, and more 100 of them at each generation.6  In other words, your child is 100 mutations worse than you, on average - despite all the effort that life does, with repair mechanisms to avoid such deleterious mutations. Perhaps, then, we have found the answer: our least 125 million bits differences were mainly caused by evil mutations. That is, yes we are "cousins" of chimpanzees, and descendants of the common ancestor ape, but we and chimpanzees really are mutant beings, and "worsened" by mutations. We "unevolved" and we were losing, for example, the hair, which warmed in the winter, and the ability to jump from branch to branch, these acrobatic skills that only apes have, and we were accumulating fat (Figure 4), and we now spend energy  with talking nonsense - women, especially - and so on. But is it so?



Chimps, our brothers ?  Sem_ty21
Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Figura 3. O galho da árvore da Vida com o ancestral comum, e dele os gorilas, chimpanzés, orangotangos e o homem. Será?

Chimps, our brothers ?  Sem_ty22

Figure 4. "involution" of common ape ancestor to the present men according to Haldane.
3. The "Argument Bill Gates." We are - argue - very similar to the monkeys; not as much morphologically - since the difference is really striking - but genetically similar. But is it so? Genetically, we are indeed a  absurd degree of different, about 33% different. But is it that even 1 or 2% or 3% or 5% they calculate, 5 would it be little difference? Or even 2% would be a true evolutionary "Big Bang" ? And the "miracles" of speech and conscience, and that "white part" in our eyes? And let's just consider the genes? And proteins do not count? Are these small differences? To illustrate the enormity of the difference in the genome, we will use what I call "argument Bill Gates" and consider as certain the "miserable" 2% they calculated a day. Imagine then that the "Bill" sends you an email announcing: "Friend, you won at the internal microsoft lottery, and of everything I have, 2% is now yours" How would you react? Would you  complain like this ? "But Bill Gates, only 2%?" Or would you jump with joy at the many millions that these 2% represent? Yes, even about 2% who underestimated, applied to the 3.2 billion base pairs (bits), would give about 80 million bits (80,000,000) differences. A  tremendous evolutionary "Big Bang" ! A 2% "a la Bill Gates" (Figure 5) which makes Haldane squirm around in his grave.




Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna13

Figure 5. The effect "Bill Gates" the difference between human and monkey genetically. Only 2% of 3.2 billion?
4. The "Argument Living Water / Watermelon / Clouds". Even if the difference between humans and apes were even those "miserable" 2%, this similarity proves what? See the argument illustrated in Figure 6. Jellyfish, watermelons and clouds are composed of 97% water. This is a fact. But what does this "apearance" shows? It shows almost nothing, just something very trivial: that things beyond different can be formed from the same material. But, through intelligent and distinct designs, completely different things can be done with only 3% difference remaining. This argument is confusing for phylogenetic analysis, and illustrates the fallacy of genomes comparison - to the "Cherry evolution," which is more "pineapple". Something that can only be sustained against an assumption: the "belief" that we evolved and that evolution is a fact - and granted. And we have-because we have - then find a culprit at all costs. And the poor monkey - who happened to be the least "unlike us" looking - was "chosen" much to distaste, I imagine. But make bad assumptions provides and forms bad scientific basis.




Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna134
Figure 6. Watermelons, clouds and Jelly fish. Very similar in composition - 97% water, but coincidentally, extremely different things have been done with the remaining 3%.
5. The "myth of the 98% genetic similarity." Compare genomes is no easy task and today no one has an accurate idea of how this can be done accurately. And the greatest difficulty comes from our little knowledge of how the information stored there is used. Despite the genomes of chimpanzees and humans are sequenced, no one can agree on what would be the best way to compare them. And not what the best program is to do this. One of the most popular methods is based on an algorithm called BLAST, which cuts the DNA (or proteins) into small segments and then try to compare these segments of both. This appears to be the most "generous" to compare two genomes, and which takes "highest possible similarity", since it does not require a genome is structured similarly to each other. What matters in BLAST is a bit of information in a genome can be found anywhere in the other genome. I have my suspects about this method, and I think the DNA is so mysterious that it will take a lot to discover an accurate comparison method, but even with the "generous" BLAST, the scientific literature shows today that the genetic difference is actually much higher that the alleged 1-2% (Nature 2005, 437, 69). Comparisons of proponents of evolution  between chimpanzees and human genomes have very exaggerated the similarities by not consider whole chromosomes, but only parts of them, as specific genes, and "relieve" the matching rules. Worse, comparisons have made use of pre-selection and filter levels before alignment and unaligned regions are usually omitted and gaps (gaps) in the alignments are often dismissed or artificially inserted. But when these "omissions" are properly considered and evaluated all impartially, the similarity has fallen dramatically and come to a measly 66% 4 or even less: 62%, making 15 in 33% or even 38% different from chimps.

In retail, for you to understand well, see one of the comparisons that have been made: the genomes of humans and chimpanzees have only 2.4 billion (76%) of almost 3.2 billion base pairs that align correctly. But to get a good alignment, 3% artificial gaps had to be introduced, there remaining 1.23% of differences represented  by pair of bases exchanged. Moreover, there are "variations in the number of copies", which causes an additional difference of 2.7%. All in all, we share a  meager similarity of only about 70% or less, or about 1/3, or 33% different (Figure 7). The worst thing is that the human genome was used as a "template" for the sequencing of the chimpanzee genome, thus assuming a priori a resemblance, which can make this "pseudosimiliarity" in fact be even lower.  Faced with 33%  maximum, or even the "paltry" 3% or 4% if you prefer, or any intermediate value between 33 and 3%, the most recent study i know of showed 12% difference, 14  evolution seems to get "naked with its hand in the pocket" without time and without any capacity to fulfill the "mission impossible" that it has been credited for: making of "Chimpanzees your brothers."
And remember also a fact that everyone in computer science knows very well. Developers are used to use a series of routines in common, and so all its programs tend to be - in terms of routines - very similar. This similarity is as high as about 80 to 90% of totally different programs. So are the remaining 10% that make all the difference. It is not  (little) like the genetic code, but the way that this information is expressed and manipulated that makes all the difference. This stupid difference we see when comparing the "pals" with "chimps". Worse, studies have shown that we are more like gorillas than chimpanzees, 18 contrarying the tree of life represented "artistically" in Figure 3.




Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna1345



Figure 7. Men and chimpanzees: immense anatomical, behavioral differences, and speech and reasoning, and a genetic"Big Bang"  that has been estimated at up to 33%.
6. The Y chromosome: A "shovel with a ton of lime " in the alleged common simian ancestry was launched recently when compared our Y chromosomes. 5 X and Y chromosomes are those that determine sex in mammals, including humans and then the chimpanzees. The  'male' Y chromosome has long been relegated to a mere evolutionary genetics relic, to the delight of feminists, because of its small size across the X and their repetitive sequences. The "Y" was then seen as containing few genes and missing those who had, and would be of evolutionary extinction route. But again, to the anger of proponents of evolution - as a mistaken forecast of evolution - it turned out that the "Y" is actually a "super Y" chromosome small but very powerful. For Majestic functions as a "genetic switch" controlling the expression of several other genes in the chromosomes. Its effect is so pronounced that the Y is causing the main differences between men and women. The sequencing of this "super Y" 5 then showed what, and through a chromosome so fundamental and majestic? It showed a brutal and humiliating difference (Figure 8  ) to the ape-man evolution. The differences are enormous, not only in size, in base pairs (genetic repertoire), but especially genetic architecture. So different that led David Page - the chimpanzee genome project coordinator - to consider that humans and chimps have "reinvented" their chromosomes Y. Outside the Y, huge differences are also found in other chromosomes at least 3: 4, 9:12, not to mention the 21, and all code.
Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna13456

Figure 8. Comparison of the Y chromosome "Chimpanzee" and their "brothers". A "measly" 100% difference.
The authors of the Nature article - shocked, i believe, but not admitting their view as a lost case - had no choice but to appeal - and ugly - for an extremely rapid evolution of the Y chromosomes of chimpanzees and humans. In this appeal they forgot  however, to inform their readers of the complete lack of time - only 6 million years - so that such genetic "mega Big Bang"  could have occurred. And the worst was also they forgot to mention that the Y in humans is extremely preserved - equal to all males - which completely contradicts the idea that the Y would be mutating and evolving rapidly. The difference was so brutal and settled so fast that the authors - amazingly - compared with the genetic differences of our Y to Y chickens, which are not mammals. According to evolution, we split the chickens to 360 million years ago. In terms Y, then we are as much like chimpanzees as  chickens.
And if we do not find that genetic code, to the anger of geneticists, are the best source of comparison, as recently made a geneticist, Eugene McCarthy of the University of Georgia, USA, but compare the anatomical similarities, a la Darwin and the nozzles of their finches, the best inference would be to be the result of breeding pigs with chimpanzees. Because we have many morphological characteristics similar to chimpanzees and also to pigs, so it seems we are both fruits of mating of both. Simple, right (Figure 9)?



Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna134567







7. Fusion of 2A + 2B chromosomes? There is still a large genetic difference between chimpanzees and humans, perhaps the most dramatic of all: humans have 23 pairs of chromosomes while the monkeys have 24. And 24 is 100% different from 23. Rationalization made to justify this "mortal difference "suggests a supposed evolutionary fusion of chromosomes 2A and 2B chimpanzee chromosome 2 in humans. It was thought then that the human chromosome 2 showed a melting point, or a kind of "genetic scar" that indicated the point where the ancestral chromosomes 2A and 2B "chimps" had merged via their telomeres, and that this scar would be proof of such a merger. But recent 6  studies have shown that there is no sign of such a scar on chromosome 2 in humans, and even more: this study presents a number of clear genetic data showing that such a merger and such scars are another two fallacies of monkey-man evolution. For example, in the supposed melting point, there is a very small number of  telomere sequences expected (TTAGGG) and few of them appear connected (in "tandem), which appears to overturn the theory of chromosomal fusion via telomeres, something never seen in life . Moreover, the "centromeres" were located in very different regions other than those prescribed.
And there is more, imagine that this merger has taken place even after we split from chimpanzees. What should we then see there? Two types of humans, a guy with 24 and other with 23 pairs of chromosomes, because the merger would have occurred to a single individual while everyone else would have continued with its 24 pairs. Moreover, it is hard to imagine a very big advantage of such a merger that  all humans with 24 chromosomes   would have  extinguished over the "super man with 23 pairs" and their descendants. That is, we are the same, it indicates 100% of chimpanzees different in terms of number of chromosome 24 because it is different  100% of 23.



Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC
Chimps, our brothers ?  Junk_dna1345678

Figure 9. The alleged fusion of 2A + 2B chromosomes of "chimps" to form the human chromosome 2.
8. Differences of protein content: 80% . The genetic differences between humans and apes, as we have seen, is gigantic and has ranged from 2% to 33%. But the vast majority of the genetic code - about 97-98% in humans - corresponds to the metadata (former "junk DNA"), which coordinates but does not express  proteins. In an article published in 2005.7 was suggested, and I as a chemist agree - that the best way to compare men with monkeys would not be using the full genomes of the two, but the end product of these genomes expressed in the form of proteins - the building blocks  of living beings. They were then compiled 127 most common proteins in humans and monkeys ("orthologous") with a total of 44 thousand amino acid sequences. And what did they find? Simply, it was discovered that humans and chimpanzees are 80% different in proteíns- as the article title 7 leaves no doubt (Figure 11).
And proteins are things so complex and finely tuned that you can not talk that a protein is virtually the same as another to have "almost" the same sequence of AA - using BLAST as a comparison method, for example - as we see in various pathologies until a simple exchange of a single AA can make the protein completely lose its function or even have quite another. This effect can be seen in the exchange of glutamic acid for valine in hemoglobin causing sickle cell anemia. Another example is the FOXP2 protein, which has only two of some 700  AAs different in chimpanzees and humans, 17 or in other words, are 99.7% similar. But FOXP2 proteins of  humans have an asparagine instead of threonine at position 303 and a serine in place of an asparagine at position 325, and these "subtle" changes makes a "tremendous" difference in their functions and the regulation of their activities via phosphorylation. Thus, a very high degree of sequence similarity may be irrelevant if the AA which is different plays a crucial role, and a single or very few AAs may become a 100% protein different from each other.




Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC

Chimps, our brothers ?  Junk_dna13456789




Figure 11. Men and chimpanzees: immense anatomical, behavioral differences, and speech and reasoning, and proteins in a mega "Big Bang" of 80%.

9. Telomeres: At the end of each chromosome, there are very complex structures known as telomeres (Figure 12) formed by RNA, DNA and various proteins and which contains DNA repeated sequences bases TTAGGG in humans. The function assigned to telomeres is to preserve the chromosomes, protecting them from degradation, recombination and fusion. Yes, melting! Its size decreases over the cell duplication to a minimum size that stops cell proliferation, which would indicate that telomeres could also function as a cellular clock controlling the "life time". Repeated sequences of telomeres do not appear, however, only at the end of chromosomes, but are seen, and very often in inner regions of DNA in various chromosomes, as in chromosome 2 and human Y. The Y chromosome has about 0.25% of its sequence TTAGGG repeats, demonstrating that these repetitions have also "internal" function, and a further layer of information in DNA. These internal sequences also demystify the supposed evidence of chromosomal fusion 2A + 2B = 2 via telomeres already discussed. Telomeres of chimpanzees and other primates have about 23 000 repeated bases. Humans are unique among primates, and have much smaller telomeres, with about 10,000 repetitions, which makes us in terms of telomeres - only considering size, beside other differences, about 67% different.






Chimps, our brothers ?  AAffA0nNPuCLAAAAAElFTkSuQmCC

Chimps, our brothers ?  Junk_dna134567890





Figure 12. The wonderful genetic engineering of telomeres, end shields of our chromosomes made up of DNA double helix tapes TTAGG repetitions, and various proteins.

10. "The pseudogene beta globin". Proponents of evolution have long used this gene as another pillar of pro-evolution argument "ape-man" and called it a "pseudogene" because "believed" it was broken. It was argued then that chimpanzees and humans - to have the same "pseudogene", shared a genetic relic from a common ancestor. But a recent study showed that this is another misconception of evolution. The remaining mutant is not  useless because it has been found that the "pseudogene" HBBP1 β-globin "gene plays multiple roles in a wide variety of tissues and cell types as a regulatory feature cleverly designed and also be highly intolerant to mutations.8

And look, we set aside other huge differences. Ariano Suassuna paraphrases or quotes Beethoven and his fifth. symphony for "not humiliating chimps". And we not also speak speech capacity and human reasoning, another evolutionary "big bang" . And it as has been shown in humans that grew enclosed, the same speech in modern humans is only developed by stimulus. How then to imagine that such capacity arose without the stimulus  from non-speaking beings? Biologists have wondered how humans and chimpanzees, as genetically  "similar" beings - the myth of 2-3% - could be so different morphologically and intellectually? Corrected in face of more recent evidence, that question would be reformulated as follows: " How could so different beings  be so different?" The answer then becomes obvious, and the question foolish . As never before, so the neo-Darwinian theory assumes that the evolutionary relationship between humans and chimpanzees today shows how an ideological delusion supported the alleged action of natural processes - natural -Selection, gene duplication and mutations occurring over millions of years - morphological superficial comparisons, and rhetorical arguments about the "why" forgetting the "how." 

And because of the fault of our nearly ignorance of the genomes of chimps and humans, their Y chromosomes, and their telomeres, and everything, evolution "monkey-man" made sense for a while. But now that paleontologists have built a huge and very detailed "Museum of Life", and geneticists have unraveled the genetic codes of the two, and calculated their incorporation rates of beneficial and deleterious mutations, and also found almost zero action of natural selection on our genomes, and everything else, delirium broke, like a mirage in the desert. Like awakening from a long delusional dream.

_______
Referências e notas
1. J. B. S. Haldane "The Cost of Natural Selection", J. Genet. 1957, 55, 511.
2. "Cost theory and the cost of substitution— a clarification" TJ 2005, 199, 113.
3. "The Biotic Message", St. Paul Science, 1995, de Walter J. ReMine.
4. "Comprehensive Analysis of Chimpanzee and Human Chromosomes Reveals Average DNA Similarity of 70%" Tomkins, J. P. Answers Research Journal. 2013, 6, 63.
5. "Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content" Jennifer F. Hughes, Helen Skaletsky, Tatyana Pyntikova, Tina A. Graves, Saskia K. M. van Daalen, Patrick J. Minx, Robert S. Fulton, Sean D. McGrath, Devin P. Locke, Cynthia Friedman, Barbara J. Trask, Elaine R. Mardis, Wesley C. Warren, Sjoerd Repping, Steve Rozen, Richard K. Wilson, David C. Page Nature, 2010, 463, 536.
6. Genomic Structure and Evolution of the Ancestral Chromosome Fusion Site in 2q13–2q14.1 and Paralogous Regions on Other Human Chromosomes Yuxin Fan, Elena Linardopoulou, Cynthia Friedman, Eleanor Williams, Barbara J. Trask Genome Research 2002, 12, 1651.
7. "Eighty percent of proteins are different between humans and chimpanzees" Galina Glazko, Vamsi Veeramachaneni, Masatoshi Nei, Wojciech MakayowskiGene , 346, 215–219, 2004.
8. "Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation" Ana Moleirinho, Susana Seixas, Alexandra M. Lopes, Celeste Bento, Maria J. Prata, António Amorim, Genome Biology and Evolution, 2013, 5, 559.
9. Ann Gauger et al. Science and Human Origins, Discovery Institute Press, June 18, 2012.
10. J. C. Sanford "Genetic Entropy & The Mistery of the Genome", Elim Publishing, New York, 2005.
11. Temos 1/3 de genes específicos em humanos quando comparados com os chimpanzés segundo esse artigo: "Mapping Human Genetic Ancestry" Ingo Ebersberger, Petra Galgoczy, Stefan Taudien, Simone Taenzer, Matthias Platzer, Arndt von Haeseler, Mol. Biol. Evol. 24, 2266, 2007.
12. "Relative Differences: The Myth of 1%" John Cohen Science 316, 1836, 2007.
14. "Documented Anomaly in Recent Versions of the BLASTN Algorithm and a Complete Reanalysis of Chimpanzee and Human Genome-Wide DNA Similarity Using Nucmer and LASTZ" Jeffrey P. Tomkins Answers Research Journal 2015, 8, 379.
15. A simple statistical test for the alleged “99% genetic identity” between humans and chimps. Uncommon Descent September 17, 2010. http://www.uncommondescent.com/intelligent-design/a-simple-statistical-test-for-the-alleged-99-genetic-identity-between-humans-and-chimps/
16. “Which of Our Genes Make Us Human?” Ann Gibbons, Science 281, 1432, 1998.
17. “Molecular Evolution of FOXP2, a Gene Involved in Speech and Language” Wolfgang Enard, Molly Przeworski, Simon E. Fisher, Cecilia S. L. Lai, Victor Wiebe, Takashi Kitano, Anthony P. Monaco, Svante Pääbo Nature 418, 869, 2002.
18. “Genetic Evidence for Complex Speciation of Humans and Chimpanzees" N. Patterson et al., ” Nature 441, 315, 2006.
19. George C. Williams - outro geneticista evolucionista famoso, "afrontando" toda uma comunidade, escreveu em seu livro "Natural Selection: Domains, Levels, and Challenges", 1992, 143-144: "The Haldane's Dilemma was never solved, by Wallace or anyone else". ou em portugues: "O dilema de Haldane nunca foi solucionado, por Wallace ou quem quer que seja".


Junk DNA' defines differences between humans and chimps
https://phys.org/news/2011-10-junk-dna-differences-humans-chimps.html

The impact of retrotransposons on human genome evolution
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884099/

Chimps, our brothers ?
https://reasonandscience.catsboard.com/t2272-chimps-our-brothers

Chimp-human-dna
https://reasonandscience.catsboard.com/t1643-chimp-human-dna

Transposons and Retrotransposons
https://reasonandscience.catsboard.com/t2393-transposons-and-retrotransposons

Early Man
http://www.detectingdesign.com/earlyman.html

Characterization and potential functional significance of human-chimpanzee large INDEL variation
https://mobilednajournal.biomedcentral.com/articles/10.1186/1759-8753-2-13



Last edited by Admin on Mon Feb 11, 2019 9:07 pm; edited 8 times in total

https://reasonandscience.catsboard.com

2Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sun Feb 07, 2016 1:54 am

Otangelo


Admin

The Evolution of Mammalian Gene Families


This chart is a great example of the insanity and corruption at work in the current scientific community.
The chart comes from the following article in PLOS: "The Evolution of Mammalian Gene Families;" Jeffery P. Demuth, Tijl De Bie, Jason E. Stajich, Nello Cristianini, Matthew W. Hahn; Published: December 20, 2006; DOI: 10.1371/journal.pone.0000085.
In the article, the authors refer to the "paradox" that chimpanzees and humans were thought to be 98.5% similar in their genes, but yet, have "substantial organismal differences". (Wow, ya really think so?) The authors refer to evidence that shows that differences in amino acids and differences in regulatory sequences contribute to the "paradox".
The article then elaborates on the fact that, since both the human genome and the chimpanzee genome have been been sequenced, it is now apparent that the chimpanzee and human genomes are not 98.5% similar, as once supposed. According to these authors' calculations, there at "at least" 1,418 genes in humans that are not in chimpanzees - 1,418 out of approximately 22,000 total genes, so humans and chimpanzees "differ by at least 6%" in their respective sets of genes. According the authors, this difference represents "a large number of genetic differences separating humans from (chimpanzees)."
Brilliant! "Science" has finally figured out what everybody else already knew - there are substantial differences between humans and chimpanzees! Hooray for science!
But now, look at this ridiculous graph. To explain the "large number of genetic differences" between humans and "our closest relatives," the authors **infer** that large numbers of genes have been gained and lost, respectively, in humans and chimpanzees since their respective descents from the "MRCA" (most recent common ancestor). How do they infer this? And why do they include this fictional graph? Because common descent is not only assumed, but now even mandated by the political establishment!
There is no evidence of a common ancestor of chimpanzees and humans. It is only assumed.
In a rare moment of honesty, a hard core proponent of universal common descent (and a PhD in Biology) posted last night, "All common ancestors are hypothetical."
HYPOTHETICAL! ALL COMMON ANCESTORS ARE HYPOTHETICAL!
So why does the scientific literature keep putting forward this fiction? Science surely is not the reason. There is a philosophical and political agenda.
What science can do - and what science **should** do - is study, analyze and enumerate the genetic and physiological differences between humans and chimpanzees (and rats and dogs and cows and so on).
What science **cannot** do - and what science should **not** do - is claim **hypothetical** common ancestors as if they were factual and refer to chimpanzees as "our closest relatives".
How about some honesty and integrity - and proper humility - from the scientific community?


Chimps, our brothers ?  Journa10

http://www.plosone.org/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0000085

https://reasonandscience.catsboard.com

3Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Wed Mar 22, 2017 7:38 pm

Otangelo


Admin

http://www.sci-news.com/othersciences/anthropology/science-homo-pan-last-common-ancestor-03220.html

A Is for . . . Adam or Ape?
https://answersingenesis.org/blogs/ken-ham/2015/09/22/a-for-adam-or-ape/

Fossil hominin shoulders support an African ape-like last common ancestor of humans and chimpanzees
http://www.pnas.org/content/112/38/11829.full



Last edited by Admin on Tue Jul 04, 2017 5:49 am; edited 1 time in total

https://reasonandscience.catsboard.com

4Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Wed Apr 05, 2017 7:02 am

Otangelo


Admin

With the sequencing of the human genome, it became clear that jumping genes—mobile genetic elements first discovered in maize by Barbara McClintock in the early 1950s—were also present and highly active during human evolution. About half of the human genome resulted from sequences of genetic code that moved or insert extra copies of themselves throughout the genome.
The evolutionary importance of jumping genes was highlighted by the results of another recent study by Gage and collaborators at Stanford. The research used stem cell technologies developed in Gage's lab to explore how differences in gene expression contribute to human and chimp facial structure. The findings, also reported in Cell, suggested that jumping genes played a role in the evolutionary split between humans and other primates.
https://phys.org/news/2015-10-scientists-protein-factories-hidden-human.html#jCp


Davide Marnetto Genome-wide Identification and Characterization of Fixed Human-Specific Regulatory Regions 2014 Jul 3

Changes in gene regulatory networks are believed to have played an important role in the development of human-specific anatomy and behavior. We identified the human genome regions that show the typical chromatin marks of regulatory regions but cannot be aligned to other mammalian genomes. Most of these regions have become fixed in the human genome. Their regulatory targets are enriched in genes involved in neural processes, CNS development, and diseases such as autism, depression, and schizophrenia. Specific transposable elements contributing to the rewiring of the human regulatory network can be identified by the creation of human-specific regulatory regions. Our results confirm the relevance of regulatory evolution in the emergence of human traits and cognitive abilities and the importance of newly acquired genomic elements for such evolution.

Empirical evidence and theoretical arguments suggest that the rewiring of gene regulatory networks plays an important role in the evolution of metazoan anatomy. The set of targets of a trans-acting regulatory element can evolve by modifying the cis-regulatory regions (RRs) to which it binds while leaving the trans element unchanged.

By integrating the genomic sequences of a large number of mammals and chromatin-state data on human cell lines, we were able to identify those human genome portions that were acquired after the split from our closest relatives and that perform a regulatory function in our genome. Many of these regions originated from mobile DNA elements, an extremely efficient vehicle for the rewiring of regulatory networks. Most of these regions have been fixed in the human genome, and their functional relevance is suggested by the strong functional characterization of their putative targets.

As originally suggested by King and Wilson, the divergence in coding sequence between human and chimpanzee seems too low to account for the extensive differences in cognitive abilities, behavior, and metabolism between the two species. It is therefore natural to postulate that a relevant part of these differences is explained by differences in gene regulation rather than in gene products. HSRRs have most likely played a role in generating such differences, as shown by the enrichment of genes involved in neural development and psychiatric diseases, such as bipolar disorder, schizophrenia, and autism.

Such strong functional characterization of human-specific regulatory regions HSRRs is to be contrasted with their rather weak selective pressure at the sequence level: this suggests a model in which regulatory rewiring is more effectively performed by the relocation of whole regulatory sequences to new genomic regions and target genes rather than by a succession of point mutations on existing sequences. This mechanism was recently shown to be largely responsible for the evolution of  Transcriptional repressor CTCF also known as 11-zinc finger protein CTCF binding in mammals.

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085640/



Last edited by Otangelo on Wed Jan 19, 2022 1:53 pm; edited 1 time in total

https://reasonandscience.catsboard.com

5Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sun Dec 02, 2018 5:52 am

Otangelo


Admin

Galina Glazko Eighty percent of proteins are different between humans and chimpanzees 29 January 2005

Comparisons of the levels of morphological and protein divergence between humans and chimps demonstrated that the level of protein divergence was too small to account for the anatomical differences between these two species. To reconcile the level of divergence between proteins and morphology, it has been proposed that morphological divergence is based mostly on changes in the mechanisms controlling gene expression and not changes in the protein-coding genes themselves. The past decades have seen major advances in developmental genetics that have changed the way we approach the origin of morphological characters. These advances have produced several generalizations about the relationship between genetics and phenotypes. Among the most widely recognized is the concept of toolbox genes, that is that different body plans are realized with a conserved set of developmental genes, namely transcription factors and signalling molecules. 4


Maria V. Suntsova Differences between human and chimpanzee genomes and their implications in gene expression, protein functions and biochemical properties of the two species 2020

The divergence between human and chimpanzee ancestors dates to approximately 6,5–7,5 million years ago. 1  human and chimpanzee genomes have multiple differences including single nucleotide substitutions, deletions and duplications of DNA fragments of different size, insertion of transposable elements and chromosomal rearrangements. Human-specific single nucleotide alterations constituted 1.23% of human DNA, whereas more extended deletions and insertions cover ~ 3% of our genome. Moreover, much higher proportion is made by differential chromosomal inversions and translocations ( Chromosome inversions are defined as the rearrangement produced by two break-points within the same chromosome, with the subsequent inversion and reinsertion of this fragment 3) comprising several megabase-long regions or even whole chromosomes. However, despite of extensive knowledge of structural genomic differences we still cannot identify with certainty the causative genes of human identity. Most structural gene-influential changes happened at the level of expression regulation, which in turn provoked larger alterations of interactome gene regulation networks.

Human karyotype is represented by 46 chromosomes, whereas chimpanzees have 48 chromosomes. In general, both karyotypes are very similar. However, there is a major difference corresponding to the human chromosome 2. It has originated due to a fusion of two ancestral acrocentric chromosomes corresponding to chromosomes 2a and 2b in chimpanzee. Also, significant pericentric inversions were found in nine other chromosomes. Two out of nine are thought to occur in human chromosomes 1 and 18, and the other seven – in chimpanzee chromosomes 4, 5, 9, 12, 15, 16 and 17. In addition, there are numerous differences in the chromosomal organization of pericentric, paracentric, intercalary and Y type heterochromatin; for example, the chimpanzees have large additional telomeric heterochromatin region on chromosome 18. Additionally, the majority of chimpanzee’s chromosomes contain subterminal constitutive heterochromatin (C-band) blocks (SCBs) that are absent in human chromosomes. SCBs predominantly consist of the subterminal satellite (StSat) repeats, they are found in African great apes but not in humans. The presence of such SCBs affects chimpanzees’ chromosomes behavior during meiosis causing persistent subtelomeric associations between homologous and non-homologous chromosomes. As a result of homologous and ectopic recombinations chimpanzees demonstrate greater chromatin variability in their subtelomeric regions.

Studying sex chromosomes also revealed several peculiar traits. There are several regions of homology between X and Y chromosomes, so-called pseudoautosomal regions (PARs) most probably arisen due to translocation of DNA from X to Y chromosome. The term “pseudoautosomal” means that they can act as autosomes being involved in recombination between X and Y chromosomes. PAR1 is a 2,6 Mb long region located at the end of Y chromosome short arm. It is homologous to the terminal region of the short arm on X chromosome. PAR2 is a 330 kb-long sequence located on the termini of long arms of X and Y chromosomes. In contrast to PAR1 presenting in many mammalian genomes, PAR2 is human-specific. It includes four genes: SPRY3, SYBL1, IL9R and CXYorf1. The first two genes (SPRY3, SYBL1) are silent on the Y chromosome (SPRY3, SYBL1) and are subjects of X-inactivation-like mechanism. On the other hand, the genes IL9R and CXYorf1 are active in both sex chromosomes. Moreover, the short arm of Y contains a 4 Mb-long translocated region from the long arm of X chromosome, called X-translocated region (XTR). A part of the XTR has undergone inversion due to recombination between the two mobile elements of LINE-1 family. Both translocation and inversion took place already after separation of human and chimpanzee ancestors [14, 58]. Finally, this region also includes genes PCDH11Y and TGIF2LY which correspond to X chromosome genes PCDH11X and TGIF2LX [15]. Around 2% of human population have signs of recombination between X and Y chromosomes at the XTR. It should be considered, therefore, as an additional human-specific pseudoautosomal region PAR3.

Conclusions
It is now generally accepted that both changes in gene regulation and alterations of protein coding sequences might have played a major role in shaping the phenotypic differences between humans and chimpanzees. In this context, complex bioinformatic approaches combining various OMICS data analyses, are becoming the key for finding genetic elements that contribute to the differences. It is also extremely important to have relevant experimental models to validate the candidate species-specific genomic alterations. The currently developing experimental methods such as obtaining pluripotent stem cells and target genome modifications, like CRISPR-CAS , open exciting perspectives for finding a “needle in haystack” that is truly important, or probably many such needles. However, at least for now using these experimental approaches for millions of species specific potentially impactful features reviewed here is impossible due to high costs and labor intensity. In turn, an alternative approach could be combining the refined data in a realistic model of human-specific development using a new generation systems biology approach trained on a functional genomic Big Data of humans and other primates. Such an approach could integrate knowledge of protein-protein interactions, biochemical pathways, spatio-temporal epigenetic, transcriptomic and proteomic patterns as well as high throughput simulation of functional changes caused by altered protein structures. The differences revealed could be also analyzed in the context of mammalian and primate-specific evolutionary trends, e.g. by using dN/dS approach to measure evolutionary rates of structural changes in proteins and enrichment by transposable elements in functional genomic loci to estimate regulatory evolution of genes. Apart from the single-gene level of data analysis, this information could be aggregated to look at the whole organismic, developmental or intracellular processes e.g. by using Gene Ontology terms enrichment analysis and quantitative analysis of molecular pathways.

In terms of nucleotide differences, the human is closer to the chimpanzee than to any other hominoid species. The early genome comparison by DNA hybridization suggested a nucleotide difference of 1–2%. However, a large portion (about 98%) of the human genome is known to be non-protein-coding DNA, and the estimate of 1–2% nucleotide difference is largely based on the comparison of non-protein-coding DNA, which has little effect on phenotypic characters. Therefore, for the general public who are interested in phenotypic differences, this is clearly misleading. A better way of measuring the genetic difference is to consider functional genes or proteins as the units of comparison, because these are the genetic units that control phenotypic characters. To do this, we compiled 127 human and chimp orthologous proteins ( An orthologous gene is a gene in different species that evolved from a common ancestor)  by speciation (44,000 amino acid residues) from GenBank. Only 25 (20%) of these proteins showed the identical amino acid sequence between humans and chimpanzees. In other words, the proportion of different proteins was 80%, in contrast to the 1–2% difference at the nucleotide level. How these differences are related to the morphological differences is unclear at present, but it is quite possible that a large proportion of phenotypic differences are caused by a relatively small number of regulatory mutations (King and Wilson, 1975) or major effect genes (Nei, 1987).

Comparisons of the levels of morphological and protein divergence between humans and chimps demonstrated that the level of protein divergence was too small to account for the anatomical differences between these two species. To reconcile the level of divergence between proteins and morphology, it has been proposed that morphological divergence is based mostly on changes in the mechanisms controlling gene expression and not changes in the protein-coding genes themselves. The past decades have seen major advances in developmental genetics that have changed the way we approach the origin of morphological characters. These advances have produced several generalizations about the relationship between genetics and phenotypes. Among the most widely recognized is the concept of toolbox genes, that is that different body plans are realized with a conserved set of developmental genes, namely transcription factors and signalling molecules.

1. http://sci-hub.st/https://www.ncbi.nlm.nih.gov/pubmed/18501470
2. https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-020-06962-8
3. https://www.sciencedirect.com/topics/medicine-and-dentistry/chromosome-inversion
4. https://sci-hub.yncjkj.com/10.1016/j.gene.2004.11.003



Last edited by Otangelo on Wed Jan 19, 2022 12:13 pm; edited 5 times in total

https://reasonandscience.catsboard.com

6Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Wed May 13, 2020 8:46 pm

Otangelo


Admin

Gennadi V. Glinsky Impacts of genomic networks governed by human-specific regulatory sequences and genetic loci harboring fixed human-specific neuro-regulatory single nucleotide mutations on phenotypic traits of Modern Humans April 18, 2020

Recent advances in identification and characterization of human-specific regulatory DNA sequences set the stage for the assessment of their global impact on physiology and pathology of Modern Humans. Gene set enrichment analyses (GSEA) of 8,405 genes linked with 35,074 human-specific neuro-regulatory single-nucleotide changes (hsSNCs) revealed a staggering breadth of significant associations with morphological structures, physiological processes, and pathological conditions of Modern Humans. Significantly enriched traits include more than 1,000 anatomically-distinct regions of the adult human brain, many different types of cells and tissues, more than 200 common human disorders and more than 1,000 records of rare diseases. Thousands of genes connected with neuro-regulatory hsSNCs have been identified, which represent essential genetic elements of the autosomal inheritance and offspring survival phenotypes. A total of 1,494 hsSNC- linked genes are associated with either autosomal dominant or recessive inheritance and 2,273 hsSNC-linked genes have been associated with premature death, embryonic lethality, as well as pre-, peri-, neo-, and post-natal lethality phenotypes of both complete and incomplete penetrance. Differential GSEA implemented on hsSNC-linked loci and associated genes identify 7,990 genes linked to evolutionary distinct classes of human-specific regulatory sequences (HSRS), expression of a majority of which (5,389 genes; 67%) is regulated by stem cell-associated retroviral sequences (SCARS). Interrogations of the MGI database revealed readily available mouse models tailored for precise experimental definitions of functional effects of hsSNCs and SCARS on genes causally affecting thousands of mammalian phenotypes and implicated in hundreds of common and rare human disorders. These observations suggest that a preponderance of human-specific traits evolved under a combinatorial regulatory control of HSRS and neuro-regulatory loci harboring hsSNCs that are fixed in humans, distinct from other primates, and located in differentially-accessible chromatin regions during brain development.

DNA sequences of coding genes defining the structure of macromolecules comprising the essential building blocks of life at the cellular and organismal levels remain highly conserved during the evolution of humans and other Great Apes . In striking contrast, a compendium of nearly hundred thousand candidate human-specific regulatory sequences (HSRS) has been assembled in recent years, thus providing further genetic and molecular evidence supporting the idea that unique to human phenotypes may result from human-specific changes to genomic regulatory sequences defined as “regulatory mutations”.

My comment: The authors, based on a naturalistic scientific framework, immediately hypothesize that the difference might be due to mutations of the gene regulatory network. But as Davidson stated:

No subcircuit functions are redundant with another, and that is why there is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135751/

Structurally, functionally, and evolutionary distinct classes of HSRS appear to cooperate in shaping developmentally and physiologically diverse human-specific genomic regulatory networks (GRNs) impacting preimplantation embryogenesis, pluripotency, and development and functions of human brain. The best evidence of the exquisite degree of accuracy of the contemporary molecular definition of human-specific regulatory sequences is exemplified by the identification of 35,074 single nucleotide changes (SNCs) that are fixed in humans, distinct from other primates, and located within differentially-accessible (DA) chromatin regions during the human brain development in cerebral organoids. Therefore, this type of mutations could be defined as fixed neuro-regulatory human-specific single nucleotide changes (hsSNCs). However, only a small fraction of identified DA chromatin peaks (600 of 17,935 DA peaks; 3.3%) manifest associations with differential expression in human versus chimpanzee cerebral organoids model of brain development, consistent with the hypothesis that regulatory effects on gene expression of these DA chromatin regions are not restricted to the early stages of brain development. 

My comment: John Sanford The waiting time problem in a model hominin population 17 September 2015
Biologically realistic numerical simulations revealed that a population of this type required inordinately long waiting times to establish even the shortest nucleotide strings. To establish a string of two nucleotides required on average 84 million years. To establish a string of five nucleotides required on average 2 billion years. We found that waiting times were reduced by higher mutation rates, stronger fitness benefits, and larger population sizes. However, even using the most generous feasible parameters settings, the waiting time required to establish any specific nucleotide string within this type of population was consistently prohibitive.
 https://tbiomed.biomedcentral.com/articles/10.1186/s12976-015-0016-z

Annotation of SNCs derived and fixed in modern humans that overlap DA chromatin regions during brain development revealed that essentially all candidate regulatory human-specific SNCs are shared with the archaic humans (35,010 SNCs; 99.8%) and only 64 SNCs are unique to modern humans (Kanton et al., 2019). This remarkable conservation on the human lineage of human-specific SNCs associated with human brain development sows the seed of interest for in-depth exploration of coding genes expression of which may be affected by genetic regulatory loci harboring human-specific SNCs.

In this contribution, the GREAT algorithm (McLean et al., 2010, 2011) was utilized to identify 8,405 hsSNCs-linked genes expression of which might be affected by 35,074 human-specific SNCs located in DA chromatin regions during brain development. Comprehensive gene set enrichment analyses (GSEA) of these genes revealed the staggering breadth of associations with physiological processes and pathological conditions of H. sapiens, including more than 1,000 anatomically-distinct regions of the adult human brain, many human tissues and cell types, more than 200 common human disorders and more than 1,000 rare diseases. It has been concluded that hsSNCs-linked genes appear contributing to development and functions of the adult human brain and other components of the central nervous system; they were defined as genetic markers of many tissues across human body and were implicated in the extensive range of human physiological and pathological conditions, thus supporting the hypothesis that phenotype-altering effects of neuro-regulatory hsSNCs are not restricted to the early-stages of human brain development. Differential GSEA implemented on hsSNC-linked loci and associated genes identify 7,990 genes linked to evolutionary distinct classes of human-specific regulatory sequences (HSRS). Notably, expression of a majority of this common set of genes (5,389 genes; 67%) is regulated by stem cell-associated retroviral sequences (SCARS). Collectively, observations reported in this contribution indicate that structurally, functionally and evolutionary diverse classes of HSRS, neuro-regulatory hsSNCs, and associated elite set of 7,990 genes affect wide spectra of traits defining both physiology and pathology of Modern Humans by asserting human-specific regulatory impacts on thousands essential mammalian phenotypes.


Gennadi V. Glinsky A Catalogue of 59,732 Human-Specific Regulatory Sequences Reveals Unique-to-Human Regulatory Patterns Associated with Virus-Interacting Proteins, Pluripotency, and Brain Development 8 Jan 2020

Analysis of 4433 genes encoding virus-interacting proteins (VIPs) revealed that 95.9% of human VIPs are components of human-specific regulatory networks that appear to operate in distinct types of human cells from preimplantation embryos to adult dorsolateral prefrontal cortex. These analyses demonstrate that modern humans captured unique genome-wide combinations of regulatory sequences, divergent subsets of which are highly conserved in distinct species of six NHP separated by 30 million years of evolution. Concurrently, this unique-to-human mosaic of genomic regulatory patterns inherited from ECAs was supplemented with 12,486 created de novo HSRS. Genes encoding VIPs appear to represent a principal genomic target of human-specific regulatory networks, which contribute to fitness of Homo sapiens and affect a functionally diverse spectrum of biological and cellular processes controlled by VIP-containing liquid-liquid phase-separated condensates.3


Shiho Endo Search for Human-Specific Proteins Based on Availability Scores of Short Constituent Sequences: Identification of a WRWSH Protein in Human Testis November 21st 2019

Little is known about protein sequences unique in humans. Here, we performed alignment-free sequence comparisons based on the availability (frequency bias) of short constituent amino acid (aa) sequences (SCSs) in proteins to search for human-specific proteins. Focusing on 5-aa SCSs (pentats), exhaustive comparisons of availability scores among the human proteome and other nine mammalian proteomes in the nonredundant (nr) database identified a candidate protein containing WRWSH, here called FAM75, as human-specific. Examination of various human genome sequences revealed that FAM75 had genomic DNA sequences for either WRWSH or WRWSR due to a single nucleotide polymorphism (SNP). FAM75 and its related protein FAM205A were found to be produced through alternative splicing. The FAM75 transcript was found only in humans, but the FAM205A transcript was also present in other mammals. In humans, both FAM75 and FAM205A were expressed specifically in testis at the mRNA level, and they were immunohistochemically located in cells in seminiferous ducts and in acrosomes in spermatids at the protein level, suggesting their possible function in sperm development and fertilization. This study highlights a practical application of SCS-based methods for protein searches and suggests possible contributions of SNP variants and alternative splicing of FAM75 to human evolution.

The human species has unique traits among animals. It is well known that morphological and physiological traits such as erect bipedalism, speech and language, and long reproductive period are very different from those of other primate species. Only humans have high intelligence that fosters sophisticated communications and complex societies. This intelligence is related to continuous brain development after birth in humans, which is not observed in  great apes, including chimpanzees. The simplest hypothesis to explain human uniqueness is that it originates from the uniqueness of constituent molecules (i.e., genes and proteins) themselves. In this “constituent hypothesis,” humans have unique genes and proteins that do not exist in chimpanzees. A contrasting hypothesis is that constituent molecules are similar between humans and chimpanzees, but they are regulated differently in these species. That is, in this “regulatory hypothesis,” a similar set of proteins may be produced but at different times (heterochrony), in different locations (heterotopy), in different amounts (heterometry), and in different usage (heterotypy). 

One line of support for the regulatory hypothesis comes from genomics and developmental expression studies. Following the announcement of a human genome release, the genomes of great apes were sequenced. Comparisons of DNA sequences between humans and chimpanzees have revealed that nucleotide differences are only 1.23% in aligned sequences, and most of these differences are thought to be functionally insignificant. Further rigorous comparisons throughout these genomes have revealed that nucleotide differences are 4% and that they are mostly located in noncoding regions. The expression patterns of some genes are different between humans and chimpanzees during development. Differences in transcriptomes have revealed that species differences in expression patterns are tissue-dependent and that testes have the greatest difference. It has been speculated that the accumulation of small expression or regulatory differences leads to large phenotypic differences between humans and chimpanzees. RNA-mediated mechanisms for novel genes have been proposed together with the “out of the testis” hypothesis, in which testis is considered a tissue for experimenting with new genes. Comparisons among transcriptomes in primates have revealed that many genes for spermatogenesis in testes, which likely inhibit apoptosis when mutated, are positively selected.

Although sequence alignment methods are powerful and probably the most important in comparison studies, sequences that do not contain relatively long regions of similarity cannot be compared well. In other words, short sequences that do not extend to longer similarities are discarded as noise. Although this strategy is highly successful, it assumes that nonaligned short sequences are not important, which may not always be true. There may still be important differences undiscovered where alignments are not possible.

Our SCS-based approach identified FAM75, a WRWSH-containing protein, as a candidate human-specific protein. Its uniqueness in humans may be acquired not only by a point mutation for WRWSH but also by novel alternative splicing. Together with FAM205A, FAM75 is likely expressed in human testis, and its possible expression in acrosomes suggests its potential function in fertilization and thus in human speciation.


Mainá Bitar Genes with human-specific features are primarily involved with brain, immune and metabolic evolution 22 November 2019 2

Here we critically update high confidence human-specific genomic variants that mostly associate with protein-coding regions and find 856 related genes.Functional analysis of these human-specific genes identifies adaptations to brain, immune and metabolic systems to be highly involved. We further show that many of these genes may be functionally associated with neural activity and generating the expanded human cortex in dynamic spatial and temporal contexts.

Functional differences between humans and primates are evident in major morphological features such as the skeleton (e.g. jaws and hands), hair (humans have thinner hair) and muscle tissue, and global functions including speech and language, changes in the brain have presumably had the most significant impact on the human lineage. The size of the human brain is triple. Comparative neuroanatomy has revealed a specific expansion of both the neocortex, with increase in size and neuronal interconnectivity during hominid evolution and the right side of the human brain compared to chimpanzee. While this expansion is believed to be important to the emergence of human language and other high-order cognitive functions, its genetic basis remains largely unknown.






1. https://www.intechopen.com/chapters/70145
2. https://bmcbioinformatics.biomedcentral.com/articles/10.1186/s12859-019-2886-2
3. https://www.liebertpub.com/doi/10.1089/dna.2019.4988
4. https://www.biorxiv.org/content/10.1101/848762v3.full

https://www.youtube.com/watch?v=FEM-80qPJHo&feature=youtu.be&fbclid=IwAR0QHkWPtyAZoe2LtBOFkRB4X8KYKNvD5OVLPHKTNbCamkWFx6gJ-Dpi5oM



Last edited by Otangelo on Tue Jan 11, 2022 9:57 pm; edited 5 times in total

https://reasonandscience.catsboard.com

7Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sat Oct 17, 2020 4:43 pm

Otangelo


Admin

No, I would not believe in something that is impossible.//
-The Y chromosome alone destroys the idea.
THE Y CHROMOSOME
Perhaps the most startling human-chimpanzee genome data of recent times, are the results from comparing DNA sequence from human and chimpanzee Y-chromosomes (Hughes et al. 2010 & 2013). Specifically, this recent study involved the comparison of the male-specific regions of the Y chromosome (MSY). While much of the human Y chromosome has been sequenced, only the MSY region of the chimpanzee Y chromosome was sequenced to a high level of completion and then compared to the corresponding region in the human Y-chromosome.
What made this study unique was that the MSY region in chimpanzee was largely assembled and constructed based on a clone-based physical map for chimpanzee, not the human physical frame-work. This allowed for a relatively reasonable comparison of the MSY sequence between human and chimp, the first time such an apparently unbiased large-scale comparison had actually been done. The results were completely unexpected and radically contradicted the standard evolutionary dogma which pervades the scientific community. The research paper title was well chosen and a very accurate one-sentence summary of the project: “Chimpanzee and human chromosomes are remarkably divergent in structure and gene content.” Perhaps the most interesting highlight of the study was the difference in gene content. While the non-genic areas between human and chimp in the MSY region were also dramatically different, the human MSY contained 78 genes while the chimpanzee only contained 37, a 48% difference in total gene content alone. In addition, the human MSY contained 27 different classes of genes (gene families/categories) while chimpanzee contained only 18; meaning that nine entire classes or gene categories were not even present in the chimpanzee MSY region. Perhaps the best way to summarize the unprecedented project is to quote some lines from the original research report.
"Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content... The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor." (excerpt from abstract, Hughes et al. 2010, p. 536)
The surprising finding of the chimpanzee Y chromosome sequence is that it contains only two-thirds the number of genes compared with the human Y chromosome. Fully 30% of the human Y chromosome contains no analogous region on the chimpanzee counterpart. In addition, the chimpanzee Y chromosome contains less than half the protein-coding genes of the human counterpart, even though it contains twice as many massive palindromes as the human. Even the parts of the Y Chromosomes that are analogous are arranged in a completely different manner.
Scientists have been rather surprised at the differences seen between the human and chimpanzee Y chromosome. Christine Disteche (University of Washington) said, "It's expected that they are going to be more different than the rest of the genome, but the extent of it is pretty amazing." According to the authors of the study, "Indeed, at 6 million years of separation, the difference in MSY gene content in chimpanzee and human is MORE COMPARABLE to the difference in autosomal gene content IN CHICKEN AND HUMAN, at 310 million years of separation." David Page (program leader at the Whitehead Institute for Biomedical Research) said, "It looks like there's been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages." He also called the chromosomes, "HORRENDOUSLY DIFFERENT FROM EACH OTHER."
Described as being "horrendously different," the sequence change is virtually unexplainable over the 6-7 million years between the hypothesized chimp-human split.
(all emphasis added)

https://reasonandscience.catsboard.com

8Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Fri Jan 22, 2021 12:36 pm

Otangelo


Admin

A part of the brain called the cerebral cortex – which plays a key role in memory, attention, awareness, and thought – contains twice as many cells in humans as the same region in chimpanzees.

"One consequence of the numerous duplications, insertions, and deletions, is that the total DNA sequence similarity between humans and chimpanzees is not 98% to 99%, but instead closer to 95% to 96%, although the rearrangements are so extensive as to render one-dimensional comparisons overly simplistic"  http://www.pnas.org/content/early/2012/06/19/1201894109.full.pdf

"one finds that the human and chimpanzee genomes are indeed about 95% identical, genome wide"
http://biologos.org/blog/adam-eve-and-human-population-genetics-part-10-addressing-criticspoythress

3-D Human Genome Radically Different from Chimp
https://www.icr.org/article/12594/

A TAD Skeptic: Is 3D Genome Topology Conserved? 13 Nov 2020,
https://www.sciencedirect.com/science/article/abs/pii/S0168952520302985

Comparative studies have reported that, genome‐wide, the overlap of the histone modification H3K4me3 locations in humans and chimpanzees is around 70%
Remarkably, the genome-wide overlap of H3K4me3 locations in humans and mouse is also around 70%

The fickle Y chromosome 13 January 2010 | Nature
The common chimp (Pan troglodytes) and human Y chromosomes are "horrendously different from each other", says David Page of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, who led the work. "It looks like there's been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages." More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa. The relationship between the human and chimp Y chromosomes has been blown to pieces."
https://www.nature.com/news/2010/100113/full/463149a.html

Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content  2013 May 14
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/

Y chromosome shock
More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome and vice versa.
https://creation.com/y-chromosome-shock

Mitochondrial Eve refuses to die
https://science.sciencemag.org/content/259/5099/1249

Eighty percent of proteins are different between humans and chimpanzees
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5745492/

https://reasonandscience.catsboard.com

9Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sat Jan 15, 2022 6:36 pm

Otangelo


Admin

A couple of years ago a list of genes in which changes had happened was presented as a series of happy accidents that led to man.
SLC2A1 and SLC2A4
CKB
HAR1 and ARHGAP11B
GADD45G
DARPP-32
SRGAP2
CHRFAM7A and PDE4DIP
Foxp2
HOXA13
AQP7
All those changes resulting in the dramatic differences between ape and man present like an intelligently designed series of strategic adjustments to create from the same genetic library.

https://reasonandscience.catsboard.com

10Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Mon Jan 24, 2022 10:31 pm

Otangelo


Admin

Fazale Rana Yeast Gene Editing Study Raises Questions about the Evolutionary Origin of Human Chromosome 2 September 12, 2018
https://reasons.org/explore/blogs/the-cells-design/yeast-gene-editing-study-raises-questions-about-the-evolutionary-origin-of-human-chromosome-2

Ryan C. Pink Pseudogenes as regulators of biological function APRIL 30 2013
Previous dogma has dictated that because the pseudogene no longer produces a protein it becomes functionless and evolutionarily inert, being neither conserved nor removed. However, recent evidence has forced a re-evaluation of this view. Some pseudogenes, although not translated into protein, are at least transcribed into RNA. In some cases, these pseudogene transcripts are capable of influencing the activity of other genes that code for proteins, thereby altering expression and in turn affecting the phenotype of the organism.
https://portlandpress.com/essaysbiochem/article-abstract/doi/10.1042/bse0540103/78236/Pseudogenes-as-regulators-of-biological-function?redirectedFrom=fulltext

https://reasonandscience.catsboard.com

11Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Tue Oct 11, 2022 11:56 am

Otangelo


Admin

The actual chimp/human similarity is only 84%. Total junk science. Real science, real scientists and real scientific papers. The 1000 Genomes Project ran between 2008 and 2015, creating the largest public catalogue of human variation and genotype data. In their
report they state, “Analysis of shared haplotype lengths around f 2 variants suggests a median common ancestor -296 generations ago (7,410 to 8,892 years ago), although those confined within a population tend to be younger with a shared common ancestor – 143 generations ago (3,570 to
4,284 years ago).” These are dates consistent with the Biblical account and not the evolution mythology. Ape to Human Evolution
According to genetics it is impossible for humans to have evolved from an ape like creature. The difference between chimp and human is not 99% but a maximum of 84% similarity. This fact falsifies the evolution of ape to man making an evolutionary process impossible.1, 2
Genetic discoveries and the human race
Genetic discoveries show that all humans and animals have an ancestral couple (Adam and Eve).3, 4, 5, 6 There was a bottleneck in the genetics and all humans are related to three families that are related to one another. (Noah's three sons and their families).7, 8, 9, 10 Geneticists have shown that the molecular dating of the human genome indicate: A bottleneck at 3,800 to 4,500 years ago (Noah's Ark)10, 11, 12, 13, 14, 15, 16 and the maximum age of the human genome is estimated to be slightly less than 6,000 years to slightly less than 9,000 years old.10, 11, 12, 13, 14, 15, 16, 17 When evolutionists date the genome they do not use todays mutation rates because they know that they indicate humans are young. They prefer to use evolutionary estimates (which have no basis in real science) and do not share this detrimental detail with the public.
The evolutionary process mutation/selection is impossible
According to genetics fixing only 8 mutations in a row would take 18 billion years which is older than the supposed universe. The information content of 8 mutations in a row is equivalent to a “Yes” or “No”. To evolve from an ape ancestor requires at least 75 million fixed mutations. (Although some suggest 120 million) 18, 19, 20
Without a naturalistic ‘Origin of Life’ there is no evolution
Origin of Life research needs to stop, says Rice University Professor of Synthetic Organic Chemistry James Tour (Voted in the top 50 of world’s most influential scientists) says, “Its over-expressed assertions jeopardize trust in scientific claims in general.” He is not the only one asking for a moratorium on Origin of Life research in that many are convinced of its impossibility for an accidental formation of biological life anywhere. Dr. Change Laura Tan and Dr. Rob Stadler (Harvard trained) suggest it has become like investing in alchemy and perpetual-motion machines. 21, 22
Geneticists now are showing humans and animals are devolving not evolving
Geneticists are showing that all life is devolving not evolving. Dr. Michael Behe reports, “Only several years ago—only after laboratory techniques were invented that could reliably track changes in species at the level of genes and DNA-was the genetic heritage of the artic predator laid bare. The results have turned the idea of evolution topsy-turvy….It seems, then that the magnificent ursus maritimus (polar bear) has adjusted to its harsh environment mainly by degrading genes that its ancestors already possessed. Despite its impressive abilities, rather than evolving, it has adapted predominantly by devolving.”
The fossils confirm that there is no real evidence for ape to man evolution
American Museum of Natural History in October 2017 said in a press release “Because fossils are so scarce, researchers do not know what the last common ancestor of living Apes and Humans looked like or where they originated.” 24 The fossil record does not show evolution but confirms that apes have always been apes and humans have always been humans.




1. Richard, Buggs, R. How similar are human and chimpanzee genomes? Posted on -R&c[0]=AT0U2vmn3imjT0B7iQnyw8jg1q--xjxljYDWU63S8aso8kvxrWgJXRLsNyPGSbf3GqHE20zgW8GQXT1da7POszlku8vAWUgPZ7J-j_1vKjTQsE1Py1ONMJk-7bEtNEj0u01ED0AABEZiJMlLRm3-xGoK]richardbugs.com
July 14, 2018.
2. Chimps and Humans; A Geneticist Discovers DNA Evidence That Challenges Evolution, Institute for Creation Research, Dallas, Texas, ICR.org
, 2021, p.p.39,46.
3. Stoeckle, S.M. and Thaler, D.S. Why should mitochondria define species? Human Evolution 33(1-2): 1-30, 2018. 10.14673/HE2018121037.
4. Jeanson, N., Replacing Darwin; The new origin of species, Master Books, Green Forest, AR, pp. 248-249, 2017.
5. The 1000 Genomes Project Consortium, A global reference for human genetic variation, 2015, Nature, 526 (7571): 68-74.
6. Venter, Craig J., Reflections on the 20th Anniversary of the First Publication of the Human Genome A new wave of research is needed to make ample use of humanity’s “most wondrous map” Scientific American, February 11, 2021.
https://www.scientificamerican.com/article/reflections-on-the-20th-anniversary-of-the-first-publication-of-the-human-genome/
7. Hood, M. Sweeping gene survey reveals new facets of evolution, Posted on PhysOrg May 28, 2018.
8. Jeanson, N.T., On the origin of human mitochondrial DNA differences, new generation time data both suggest a unified young-earth creation model and challenge the evolutionary out –of Africa model, ARJ 9:123-130, 2016.
9. Ibid 3.
10. Sanford, J. C., and R. W. Carter. 2014. In Light of Genetics…Adam, Eve, and the Creation/Fall. Christian Apologetics Journal. 12 (2): 51-98.
11. Madrigal, L. et al. 2012. High mitochondrial mutation rates estimated from deep-rooting Costa Rican pedigrees. American Journal of Physical Anthropology. 148 (3): 327-333.
12. Gibbons, A., Calibrating the mitochondrial clock, Science 279:28-29, 1998. -R&c[0]=AT0U2vmn3imjT0B7iQnyw8jg1q--xjxljYDWU63S8aso8kvxrWgJXRLsNyPGSbf3GqHE20zgW8GQXT1da7POszlku8vAWUgPZ7J-j_1vKjTQsE1Py1ONMJk-7bEtNEj0u01ED0AABEZiJMlLRm3-xGoK]http://www.dnai.org/teacherguide/pdf/reference_romanovs.pdf
.
13. Ibid 4.
14. Fu, W. et al., Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants, Nature 493:216-220, 2013 doi 10.1038/nature11690.
15. Parsons, T.J. et al., A high observed substitution rate in the human mitochondrial DNA control region, Nat Genet 15:363-368, 1997 doi:10.1038/ng0497-363.
16. Tennessen, J. A. et al, Evolution and functional impact of rare coding variation from deep sequencing of human exomes, Science 337:64-69, 2012 doi:10.1126/science. 1219240.
17. Ibid 5.
18. Sanford, J. et al., The waiting time problem in model hominin population, Theoretical Biology and Medical Modeling, 12:18, 2015 Doi:10.1186 /s12976-015-0016-z
19. Keightley P.D. and Lynch, M., Toward a realistic model of mutations affecting fitness, Evolution 57(3):683-5, 2003.
20. Kondrashov, A.S., Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? J. Theor. Biol. 175(4):583-594, 21 Aug 1995.
21. Tour, James, We’re Still Clueless about the Origin of Life, The Mystery of Life’s Origin: The Continuing Controversy, ed. Charles B. Thaxton et al., New Expanded Edition (Seattle: Discovery Institute, 2020), 323-357.
22. Change Laura Tan, Stadler, Rob, The Stairway to Life, An Origin-Of-Life Reality check, Change Laura Tan and Rob Stadler, 2020, p.216.
23. Behe, Michael J.: Darwin Devolves, The New Science About DNA That Challenges Evolution, Harper Collins, 2019, pp. 16-17. (Professor of biochemistry at Lehigh University)
24. New Study Suggests that Last Common Ancestor of Humans and Apes Was Smaller than Thought. American Museum of Natural History press release. Posted on amnh.org
October 12, 2017.


Chimps, our brothers ?  31147510

https://reasonandscience.catsboard.com

12Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Mon Oct 31, 2022 6:33 pm

Otangelo


Admin

Gennadi V. Glinsky Impacts of genomic networks governed by human-specific regulatory sequences and genetic loci harboring fixed human-specific neuro-regulatory single nucleotide mutations on phenotypic traits of Modern Humans April 18, 2020

Recent advances in identification and characterization of human-specific regulatory DNA sequences set the stage for the assessment of their global impact on physiology and pathology of Modern Humans. Gene set enrichment analyses (GSEA) of 8,405 genes linked with 35,074 human-specific neuro-regulatory single-nucleotide changes (hsSNCs) revealed a staggering breadth of significant associations with morphological structures, physiological processes, and pathological conditions of Modern Humans. Significantly enriched traits include more than 1,000 anatomically-distinct regions of the adult human brain, many different types of cells and tissues, more than 200 common human disorders and more than 1,000 records of rare diseases. Thousands of genes connected with neuro-regulatory hsSNCs have been identified, which represent essential genetic elements of the autosomal inheritance and offspring survival phenotypes. A total of 1,494 hsSNC- linked genes are associated with either autosomal dominant or recessive inheritance and 2,273 hsSNC-linked genes have been associated with premature death, embryonic lethality, as well as pre-, peri-, neo-, and post-natal lethality phenotypes of both complete and incomplete penetrance. Differential GSEA implemented on hsSNC-linked loci and associated genes identify 7,990 genes linked to evolutionary distinct classes of human-specific regulatory sequences (HSRS), expression of a majority of which (5,389 genes; 67%) is regulated by stem cell-associated retroviral sequences (SCARS). Interrogations of the MGI database revealed readily available mouse models tailored for precise experimental definitions of functional effects of hsSNCs and SCARS on genes causally affecting thousands of mammalian phenotypes and implicated in hundreds of common and rare human disorders. These observations suggest that a preponderance of human-specific traits evolved under a combinatorial regulatory control of HSRS and neuro-regulatory loci harboring hsSNCs that are fixed in humans, distinct from other primates, and located in differentially-accessible chromatin regions during brain development.

DNA sequences of coding genes defining the structure of macromolecules comprising the essential building blocks of life at the cellular and organismal levels remain highly conserved during the evolution of humans and other Great Apes . In striking contrast, a compendium of nearly hundred thousand candidate human-specific regulatory sequences (HSRS) has been assembled in recent years, thus providing further genetic and molecular evidence supporting the idea that unique to human phenotypes may result from human-specific changes to genomic regulatory sequences defined as “regulatory mutations”.

My comment: The authors, based on a naturalistic scientific framework, immediately hypothesize that the difference might be due to mutations of the gene regulatory network. But as Davidson stated:

No subcircuit functions are redundant with another, and that is why there is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135751/

Structurally, functionally, and evolutionary distinct classes of HSRS appear to cooperate in shaping developmentally and physiologically diverse human-specific genomic regulatory networks (GRNs) impacting preimplantation embryogenesis, pluripotency, and development and functions of human brain. The best evidence of the exquisite degree of accuracy of the contemporary molecular definition of human-specific regulatory sequences is exemplified by the identification of 35,074 single nucleotide changes (SNCs) that are fixed in humans, distinct from other primates, and located within differentially-accessible (DA) chromatin regions during the human brain development in cerebral organoids. Therefore, this type of mutations could be defined as fixed neuro-regulatory human-specific single nucleotide changes (hsSNCs). However, only a small fraction of identified DA chromatin peaks (600 of 17,935 DA peaks; 3.3%) manifest associations with differential expression in human versus chimpanzee cerebral organoids model of brain development, consistent with the hypothesis that regulatory effects on gene expression of these DA chromatin regions are not restricted to the early stages of brain development. 

https://reasonandscience.catsboard.com

13Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Mon Oct 31, 2022 6:36 pm

Otangelo


Admin

https://reasonandscience.catsboard.com/t2585-the-waiting-time-problem-in-a-model-hominin-population#9160


The research by Gennadi V. Glinsky and Shiho Endo provide evidence against the theory of common ancestry between humans and apes. Glinsky's study reveals that human-specific regulatory networks operate in distinct types of human cells, including brain development and pluripotency, that are not found in any other primates. These regulatory patterns inherited from ECAs were supplemented with thousands of de novo HSRS, which only exist in humans. Similarly, Endo's research identified a protein called FAM75, which is unique to humans due to a single nucleotide polymorphism and is involved in sperm development and fertilization. These findings support the constituent hypothesis that humans have unique genes and proteins that do not exist in chimpanzees, rather than the regulatory hypothesis that they are similar but regulated differently in these species. Furthermore, comparisons of DNA sequences and transcriptomes between humans and chimpanzees have revealed significant differences in expression patterns during development and in tissue-dependent areas such as the testes.

Gennadi V. Glinsky A Catalogue of 59,732 Human-Specific Regulatory Sequences Reveals Unique-to-Human Regulatory Patterns Associated with Virus-Interacting Proteins, Pluripotency, and Brain Development 8 Jan 2020

Analysis of 4433 genes encoding virus-interacting proteins (VIPs) revealed that 95.9% of human VIPs are components of human-specific regulatory networks that appear to operate in distinct types of human cells from preimplantation embryos to adult dorsolateral prefrontal cortex. These analyses demonstrate that modern humans captured unique genome-wide combinations of regulatory sequences, divergent subsets of which are highly conserved in distinct species of six NHP separated by 30 million years of evolution. Concurrently, this unique-to-human mosaic of genomic regulatory patterns inherited from ECAs was supplemented with 12,486 created de novo HSRS. Genes encoding VIPs appear to represent a principal genomic target of human-specific regulatory networks, which contribute to fitness of Homo sapiens and affect a functionally diverse spectrum of biological and cellular processes controlled by VIP-containing liquid-liquid phase-separated condensates.3


Shiho Endo Search for Human-Specific Proteins Based on Availability Scores of Short Constituent Sequences: Identification of a WRWSH Protein in Human Testis November 21st 2019

Little is known about protein sequences unique in humans. Here, we performed alignment-free sequence comparisons based on the availability (frequency bias) of short constituent amino acid (aa) sequences (SCSs) in proteins to search for human-specific proteins. Focusing on 5-aa SCSs (pentats), exhaustive comparisons of availability scores among the human proteome and other nine mammalian proteomes in the nonredundant (nr) database identified a candidate protein containing WRWSH, here called FAM75, as human-specific. Examination of various human genome sequences revealed that FAM75 had genomic DNA sequences for either WRWSH or WRWSR due to a single nucleotide polymorphism (SNP). FAM75 and its related protein FAM205A were found to be produced through alternative splicing. The FAM75 transcript was found only in humans, but the FAM205A transcript was also present in other mammals. In humans, both FAM75 and FAM205A were expressed specifically in testis at the mRNA level, and they were immunohistochemically located in cells in seminiferous ducts and in acrosomes in spermatids at the protein level, suggesting their possible function in sperm development and fertilization. This study highlights a practical application of SCS-based methods for protein searches and suggests possible contributions of SNP variants and alternative splicing of FAM75 to human evolution.

The human species has unique traits among animals. It is well known that morphological and physiological traits such as erect bipedalism, speech and language, and long reproductive period are very different from those of other primate species. Only humans have high intelligence that fosters sophisticated communications and complex societies. This intelligence is related to continuous brain development after birth in humans, which is not observed in  great apes, including chimpanzees. The simplest hypothesis to explain human uniqueness is that it originates from the uniqueness of constituent molecules (i.e., genes and proteins) themselves. In this “constituent hypothesis,” humans have unique genes and proteins that do not exist in chimpanzees. A contrasting hypothesis is that constituent molecules are similar between humans and chimpanzees, but they are regulated differently in these species. That is, in this “regulatory hypothesis,” a similar set of proteins may be produced but at different times (heterochrony), in different locations (heterotopy), in different amounts (heterometry), and in different usage (heterotypy). 

One line of support for the regulatory hypothesis comes from genomics and developmental expression studies. Following the announcement of a human genome release, the genomes of great apes were sequenced. Comparisons of DNA sequences between humans and chimpanzees have revealed that nucleotide differences are only 1.23% in aligned sequences, and most of these differences are thought to be functionally insignificant. Further rigorous comparisons throughout these genomes have revealed that nucleotide differences are 4% and that they are mostly located in noncoding regions. The expression patterns of some genes are different between humans and chimpanzees during development. Differences in transcriptomes have revealed that species differences in expression patterns are tissue-dependent and that testes have the greatest difference. It has been speculated that the accumulation of small expression or regulatory differences leads to large phenotypic differences between humans and chimpanzees. RNA-mediated mechanisms for novel genes have been proposed together with the “out of the testis” hypothesis, in which testis is considered a tissue for experimenting with new genes. Comparisons among transcriptomes in primates have revealed that many genes for spermatogenesis in testes, which likely inhibit apoptosis when mutated, are positively selected.

Although sequence alignment methods are powerful and probably the most important in comparison studies, sequences that do not contain relatively long regions of similarity cannot be compared well. In other words, short sequences that do not extend to longer similarities are discarded as noise. Although this strategy is highly successful, it assumes that nonaligned short sequences are not important, which may not always be true. There may still be important differences undiscovered where alignments are not possible.

Our SCS-based approach identified FAM75, a WRWSH-containing protein, as a candidate human-specific protein. Its uniqueness in humans may be acquired not only by a point mutation for WRWSH but also by novel alternative splicing. Together with FAM205A, FAM75 is likely expressed in human testis, and its possible expression in acrosomes suggests its potential function in fertilization and thus in human speciation.


Mainá Bitar Genes with human-specific features are primarily involved with brain, immune and metabolic evolution 22 November 2019 2

Here we critically update high confidence human-specific genomic variants that mostly associate with protein-coding regions and find 856 related genes.Functional analysis of these human-specific genes identifies adaptations to brain, immune and metabolic systems to be highly involved. We further show that many of these genes may be functionally associated with neural activity and generating the expanded human cortex in dynamic spatial and temporal contexts.

Functional differences between humans and primates are evident in major morphological features such as the skeleton (e.g. jaws and hands), hair (humans have thinner hair) and muscle tissue, and global functions including speech and language, changes in the brain have presumably had the most significant impact on the human lineage. The size of the human brain is triple. Comparative neuroanatomy has revealed a specific expansion of both the neocortex, with increase in size and neuronal interconnectivity during hominid evolution and the right side of the human brain compared to chimpanzee. While this expansion is believed to be important to the emergence of human language and other high-order cognitive functions, its genetic basis remains largely unknown.



Last edited by Otangelo on Wed Mar 15, 2023 11:38 am; edited 1 time in total

https://reasonandscience.catsboard.com

14Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Mon Oct 31, 2022 9:24 pm

Otangelo


Admin

https://www.icr.org/article/human-genome-radically-different-from-chimp

the Y chromosome shows extreme differences that can not be accounted for in chimps and humans !!

https://reasonandscience.catsboard.com

15Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Fri Sep 08, 2023 3:36 pm

Otangelo


Admin

1. Shared DNA between Species

Claim: "It’s common sense, 96% of our DNA is shared with chimpanzees. For context, chimps and gorillas share only 80%."
Response: Shared genetic material, while often cited as evidence of common ancestry, can also be viewed from a design efficiency perspective. If there exists a designer, it would make sense to utilize similar genetic blueprints across varied species, tweaking and modifying as required, much like how engineers use foundational principles across various designs. Moreover, the 4% genetic difference between humans and chimps translates to around 120 million base pairs – a significant number that can result in vast phenotypic differences.

2. Anatomical Features as Design Flaws

Claim: "If life is designed why is the fuel intake and air intake the same hole, a basic and egregious design flaw?"
Response: What might be perceived as a design flaw from one perspective might be seen as a feature of efficiency or multi-functionality from another. The shared pathways in our anatomy (like the pharynx serving both digestion and respiration) might be a testament to the principle of efficient design. Moreover, the potential "flaw" may be outweighed by other benefits that the specific design confers, such as vocalization.

The studies,  specifically those by Gennadi V. Glinsky and Shiho Endo, represent significant advances in our understanding of human-specific regulatory sequences and proteins, respectively. These findings are profound as they challenge the established idea of common ancestry between humans and apes, a cornerstone of evolutionary biology. 

Human-Specific Regulatory Sequences: Glinsky's work uncovers that human-specific regulatory networks play pivotal roles in crucial biological processes, from embryonic stages to adult brain development. Such specificity, not found in other primates, is evidence that humans have regulatory mechanisms entirely distinct from those in our closest primate relatives. When we consider the vast number of de novo HSRS (human-specific regulatory sequences) Glinsky mentions, it's evident that these aren't minor deviations but rather substantial changes that can't be explained merely by shared common ancestry.

Unique Human Proteins: Endo's research illuminates the presence of proteins, like FAM75, that are unique to humans. The fact that such a protein arose due to a single nucleotide polymorphism and yet plays a potential role in vital processes like sperm development and fertilization is intriguing. This suggests that there were specific and possibly guided changes in the human genome, leading to unique functionalities.

The existence of exclusive human genes and proteins defies the idea that humans and apes merely have regulatory differences.

Genome Comparisons and Their Limitations: While DNA sequence comparisons between humans and chimpanzees show minor nucleotide differences, the emphasis on aligned sequences potentially ignores significant genomic regions that account for the pronounced differences between the two species. And, as highlighted, methods that depend on sequence alignment might overlook short sequences that don't have longer similarities. Such sequences, previously dismissed as noise, hold the key to understanding some profound differences between species.

Brain Evolution and Uniqueness: The remarkable expansion and intricacies of the human brain, as mentioned in Mainá Bitar's work, remain one of the most profound distinctions between humans and other primates. While the genetic underpinnings of this expansion are yet to be fully understood, it's evident that simple shared ancestry might not account for these significant changes.

Shiho Endo, Kenta Motomura, Masakazu Tsuhako, Yuki Kakazu, Morikazu Nakamura, & Joji M. Otaki (2019). Search for Human-Specific Proteins Based on Availability Scores of Short Constituent Sequences: Identification of a WRWSH Protein in Human Testis. Link.
Gennadi V. Glinsky (2020). A Catalogue of 59,732 Human-Specific Regulatory Sequences Reveals Unique-to-Human Regulatory Patterns Associated with Virus-Interacting Proteins, Pluripotency, and Brain Development. Link.
Mainá Bitar (2019). Genes with human-specific features are primarily involved with brain, immune, and metabolic evolution. Link.

https://reasonandscience.catsboard.com

16Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Tue Sep 12, 2023 7:54 am

Otangelo


Admin

Distinct Human Regulatory Networks: The study by Gennadi V. Glinsky highlighted that humans have unique regulatory networks operating in diverse cell types, from embryos to the adult brain. These patterns aren't found in other primates. The presence of these human-specific regulatory sequences (HSRS) that have no analog in other primates suggests a unique genetic structure and regulatory patterns exclusive to humans.

Unique Proteins in Humans: Shiho Endo's research brought to light a protein, FAM75, which is uniquely human. This protein was detected due to a specific short constituent amino acid sequence (WRWSH) present only in humans. This uniqueness arises not just from a single nucleotide polymorphism but also from a novel alternative splicing pattern. The expression of FAM75 and its associated protein FAM205A, primarily in the human testis and its potential involvement in fertilization, implies it plays a pivotal role in human reproduction that is distinct from other species.

Unique Traits in Humans: The human species showcases specific traits not found in other animals, especially when considering bipedalism, speech, language, and sophisticated cognitive abilities. If these characteristics arose from entirely distinct molecules or gene sequences, it supports the polyphyly perspective that humans have a unique origin, separate from other primates.

DNA Sequence Comparisons: While the nucleotide difference between humans and chimpanzees is relatively low, most of these differences are concentrated in noncoding regions. The variations in expression patterns, especially those seen in the testes, indicate considerable genomic distinctions between humans and chimpanzees. This difference in expression patterns can be seen as indicative of separate genetic blueprints.

Human-specific Features in Genes: Mainá Bitar's research identified a substantial number of human-specific genomic variants. These are particularly prevalent in genes associated with brain, immune, and metabolic systems. Such distinct genetic markers in critical functions point towards a unique genetic identity and origin for humans.

Brain Differences: Humans exhibit an expanded neocortex and increased neuronal interconnectivity. These anatomical distinctions have been linked to unique cognitive capabilities, including language. Such significant divergence in brain anatomy and function supports the idea of separate origins.

Given this evidence, polyphyly presents a more case-adequate explanation because it directly addresses the distinct genetic, molecular, and physiological features exclusive to humans. The unique regulatory networks, proteins, and gene expression patterns observed in humans underscore a separate genetic blueprint, suggesting a distinct origin from apes. In this view, rather than envisioning a shared evolutionary ancestor from which both species diverged, polyphyly posits two parallel and independent origins, explaining the pronounced differences in genetic and phenotypic features between humans and apes.

https://reasonandscience.catsboard.com

17Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Tue Sep 12, 2023 7:57 am

Otangelo


Admin

1. King, M.C. & Wilson, A.C. (1975). Evolution at two levels in humans and chimpanzees. Science, 188(4184), 107-116. Link. (This classic study proposed that while protein sequences between humans and chimpanzees are largely similar, the regulatory genes controlling these proteins might have differences, possibly explaining some of our unique human traits.)

2. Varki, A., Altheide, T.K. (2005). Comparing the human and chimpanzee genomes: searching for needles in a haystack. Genome Research, 15(12), 1746-1758. Link. (This paper emphasizes the challenges and approaches of understanding human uniqueness by comparing the chimpanzee and human genomes.)

3. Green, R.E., et al. (2010). A Draft Sequence of the Neandertal Genome. Science, 328(5979), 710-722. Link. (This research provides a draft sequence of the Neandertal genome, offering insights into the divergence of Neandertals and modern humans.)

4. Prüfer, K., et al. (2017). A high-coverage Neandertal genome from Vindija Cave in Croatia. Science, 358(6363), 655-658. Link. (This paper presents a high-quality Neandertal genome and analyzes genetic overlap with modern humans.)

5. Sankararaman, S., et al. (2014). The genomic landscape of Neanderthal ancestry in present-day humans. Nature, 507(7492), 354-357. Link. (This research delves into the genomic evidence of Neandertal ancestry in modern humans, shedding light on potential interbreeding events.)

6. Sudmant, P.H., et al. (2015). An integrated map of structural variation in 2,504 human genomes. Nature, 526(7571), 75-81. Link. (The study provides a comprehensive analysis of structural variation in human genomes, which may contribute to understanding differences within and between species.)

7. Rogers, J., et al. (2019). The comparative genomics and complex population history of Papio baboons. Science Advances, 5(1), eaau6947. Link. (This research examines the genomics of Papio baboons, offering comparative insights into primate evolution.)

8. Miga, K.H., et al. (2020). Telomere-to-telomere assembly of a complete human X chromosome. Nature, 585(7823), 79-84. Link. (A landmark study that achieved a complete assembly of the human X chromosome, with implications for genetic research.)

https://reasonandscience.catsboard.com

Otangelo


Admin

The Brain of Homo Sapiens and Chimps: Distinctive Characteristics are reasons to be skeptic about shared descent

Understanding where one species ends and another begins poses an intriguing challenge. A pivotal area of study in this regard is the demarcation between humans and their closest living relatives, the apes. At a glance, humans and chimps, our closest genetic relatives, appear to have a striking DNA resemblance, with a similarity range of 98-99%. However, this small percentage of difference holds significant weight. One of the most defining differences lies in the number of chromosomes: humans have 23 pairs, while apes have 24. This key distinction is just the tip of the iceberg, with the genetic contrasts laying the groundwork for the variances we observe in anatomy, cognition, and behavior. Anatomical differences extend beyond the obvious disparities in facial structure, limb proportions, and posture. One crucial distinction lies in the neural realm. Humans possess notably specialized brain regions, like Broca's and Wernicke's areas, which are deeply intertwined with speech production and intricate language processing. Though apes have analogous regions, the level of development, sophistication, and specialization in humans is unparalleled.

The anatomical disparities between humans and apes, while rooted in genetics, are also influenced by a combination of factors: Differences in gene expression patterns during development can lead to significant anatomical changes. Even if humans and apes share many of the same genes, the timing, duration, and intensity of gene expres​sion(a phenomenon known as heterochrony) can influence the shape, size, and function of various organs and structures. Epigenetic modifications are chemical changes to the DNA molecule or associated proteins that affect gene activity without altering the DNA sequence itself. These modifications can be influenced by environmental factors and can play a role in determining traits. For example, diet, exposure to physical activity, or environmental stresses can influence epigenetic factors which, in turn, can lead to anatomical differences.

Chimpanzees have a cranial capacity of around 300-500 cc, while modern humans possess a cranial capacity of about 1350 cc. This threefold difference doesn't just imply a larger brain but reflects significant differences in brain architecture and complexity.

Broca's and Wernicke's Areas: Humans have distinct brain regions (Broca's and Wernicke's areas) linked to speech production and language processing. While primates have similar regions, they aren't as developed or specialized. A transition here isn't simply about increasing brain size but involves the instantiation of new neural structures and pathways. Broca's and Wernicke's Areas: Hallmarks of Human Linguistic Ability. Broca's and Wernicke's areas stand out as specialized centers for language processing. Found in the left hemisphere of the brain in most right-handed individuals, these regions play pivotal roles in our ability to produce and comprehend language. Broca's area, located in the frontal lobe, is primarily associated with the production of speech. Damage to this region can result in Broca's aphasia, a condition where individuals can comprehend language but struggle with fluent speech production. They might omit small connecting words like "is" or "and," resulting in what's termed "telegraphic speech." In contrast, Wernicke's area is situated in the temporal lobe and is primarily responsible for the comprehension of speech. Impairments in this area lead to Wernicke's aphasia, where speech is fluent but often nonsensical. Affected individuals might string unrelated words together, unaware that their sentences don't make sense. While primates, like chimps, exhibit regions in their brains that are somewhat analogous to Broca's and Wernicke's areas, there are notable differences. The complexity, sophistication, and specialization of these areas in humans far surpass those in primates. While primates have the capability to produce a range of vocalizations and can even understand a limited set of sign language symbols in experimental conditions, their linguistic abilities pale in comparison to the depth, range, and nuance of human language.

Furthermore, it's not just about the presence of these regions but also their connectivity and the intricate web of neural pathways that connect them. The arcuate fasciculus, a bundle of nerve fibers, connects Broca's and Wernicke's areas, enabling seamless integration of speech production and comprehension. This specialized network doesn't exist in the same way in our primate relatives.

The emergence of these advanced linguistic areas is not a simple matter of evolutionary scaling up. It's not just about having a bigger brain but rather the development of new, specialized structures and networks. The presence and intricacy of these areas in the human brain, coupled with our unparalleled linguistic abilities, raises profound questions about the direct evolutionary pathway that is often proposed between humans and our closest primate relatives. It suggests that there might be more to the story of our neural evolution, with distinct developments that uniquely define the human experience.


White Matter and Connectivity: Homo sapiens has more extensive white matter, implying enhanced connectivity between brain regions. The corpus callosum, which connects the two brain hemispheres, is more robust in humans. This isn't something that can easily "expand" in a linear evolutionary step from a chimpanzee-like ancestor.
Cognitive Abilities: Humans can think abstractly, plan for the long term, and understand complex moral and philosophical concepts. This ability goes beyond just having a bigger brain; it suggests a qualitative change in how the brain processes information. While chimps show signs of tool use and basic problem solving, they haven't demonstrated the ability to, for instance, create art, compose music, or understand complex symbols in the way humans do.
For a clear borderline: Imagine if we had to change the architecture of a contemporary computer to give it significantly more advanced capabilities. It's not just about adding more RAM or a faster processor, but the motherboard itself, the software codes, and the interaction between various components might need an overhaul. If you just increase the RAM without changing anything else, the computer might not run efficiently or even fail. Similarly, evolving from a chimpanzee-like brain to a Homo sapiens brain isn't merely about expanding what's there. It involves intricate changes at various levels, from genetic to structural to functional. A chimp's brain cannot simply "expand" to become a human brain; it would need a coordinated overhaul of many systems:

1 Cerebral Cortex: Particularly the prefrontal cortex in humans is significantly larger in relation to body size compared to chimps. This expansion supports higher cognitive functions such as reasoning and decision-making.
2 Brain Connectivity: The human brain exhibits advanced connectivity, especially in dendritic spines and synaptic connections. Differences are also notable in the white matter tracts connecting various brain regions.
3 Gyrification: The human brain is characterized by increased gyrification, with more folds and grooves, allowing a larger surface area for the cerebral cortex, supporting complex cognitive functions.
4 Language Centers: The Broca's and Wernicke's areas in humans are specialized for speech and language, while in chimps, analogous regions exist but are less developed.
5 Brain Chemistry: Differences emerge in the levels and activity of neurotransmitters and neuromodulators, which affect various cognitive and mood functions.
6 Growth and Development: Humans experience prolonged childhood and slower brain development, facilitating extended learning and cultural adaptation.
7 Brain-to-Body Ratio: Humans have a distinctively larger brain-to-body ratio, emphasizing not just size but functional capacities and energy allocation.
8 Functional Specialization: Humans have regions in the brain that are more functionally specialized, and dedicated to specific tasks or processes.
9 Metabolic Rate: The energy consumption of the human brain is notably high, reflecting its heightened activity and intricate nature.
10 Genetic Influences: Differences in the regulation of genes related to brain development and function have driven the separate evolutionary paths of humans and chimps.

This complexity and the seemingly insurmountable gap between chimp and human cognition is what points to evidence for design that is both intelligent and purposeful.

The studies,  specifically those by Gennadi V. Glinsky and Shiho Endo, represent significant advances in our understanding of human-specific regulatory sequences and proteins, respectively. These findings are profound as they challenge the established idea of common ancestry between humans and apes, a cornerstone of evolutionary biology. 

Human-Specific Regulatory Sequences: Glinsky's work uncovers that human-specific regulatory networks play pivotal roles in crucial biological processes, from embryonic stages to adult brain development. Such specificity, not found in other primates, is evidence that humans have regulatory mechanisms entirely distinct from those in our closest primate relatives. When we consider the vast number of de novo HSRS (human-specific regulatory sequences) Glinsky mentions, it's evident that these aren't minor deviations but rather substantial changes that can't be explained merely by shared common ancestry.
Unique Human Proteins: Endo's research illuminates the presence of proteins, like FAM75, that are unique to humans. The fact that such a protein arose due to a single nucleotide polymorphism and yet plays a potential role in vital processes like sperm development and fertilization is intriguing. This suggests that there were specific and possibly guided changes in the human genome, leading to unique functionalities.

The existence of exclusive human genes and proteins defies the idea that humans and apes merely have regulatory differences.

Genome Comparisons and Their Limitations: While DNA sequence comparisons between humans and chimpanzees show minor nucleotide differences, the emphasis on aligned sequences potentially ignores significant genomic regions that account for the pronounced differences between the two species. And, as highlighted, methods that depend on sequence alignment might overlook short sequences that don't have longer similarities. Such sequences, previously dismissed as noise, hold the key to understanding some profound differences between species.
Brain Evolution and Uniqueness: The remarkable expansion and intricacies of the human brain, as mentioned in Mainá Bitar's work, remain one of the most profound distinctions between humans and other primates. While the genetic underpinnings of this expansion are yet to be fully understood, it's evident that these significant changes raise doubt and skepticism about common ancestry.

1. Cerebral Cortex

In Homo sapiens, the prefrontal cortex, a part of the cerebral cortex, is considerably larger when compared to its size in apes. This allows for enhanced cognitive functions such as complex problem-solving, advanced reasoning, and decision-making. Apes, while having a developed prefrontal cortex, don't match the capabilities of humans in these cognitive areas. The human cerebral cortex, especially the prefrontal cortex, is a marvel of complexity and functionality. Its vast expansion in humans, as compared to chimps, supports advanced cognitive functions such as reasoning, decision-making, and many more intricate processes. Consider the intricate web of signaling pathways, specialized proteins, and cellular mechanisms needed for the prefrontal cortex to function. For the cortex to merely exist, there needs to be a harmonious collaboration of myriad components, each essential for the functioning and integration of neural circuits. For instance, there's the formation and modulation of synapses, intricate ion channel functions, and specialized neurotransmitter release and uptake mechanisms. Now, consider the hypothesis that each of these complexities evolved in a stepwise fashion. In an evolutionary process where beneficial traits are selected because they provide an advantage, it's challenging to imagine how intermediate stages of such sophisticated systems could confer any advantage at all. What would be the purpose of an incomplete signaling pathway, or a half-formed synaptic structure? An intermediary, non-functional stage of these systems would not confer any survival advantage and, in evolutionary terms, should be selected against. Furthermore, the cerebral cortex doesn’t just operate in isolation. It's integrated with other parts of the brain and the body. Any evolutionary change to the cortex would also necessitate corresponding changes elsewhere to maintain coherent functioning. Think of it as a complex dance where every move is synchronized. If one dancer changes their move set without the other dancers adjusting in kind, the entire choreography falls apart. The language of the brain is another astonishing complexity. Neurons communicate using intricate codes, not just simple on-off signals. This language must have been in place from the outset for effective communication. An incomplete or rudimentary neural code would be akin to having a computer with only half its programming language—it wouldn't function. The sheer number of specialized proteins and their complex interactions in the brain are staggering. Each of these proteins has to be precisely tailored to its function. A partially evolved protein, not quite fit for its eventual purpose, would be of little use, and could even be detrimental. Given these considerations, it's hard to conceive how the intricate, interconnected mechanisms of the human cerebral cortex, especially the prefrontal cortex, could have arisen through a series of small, independent steps. The apparent need for a multitude of components to be in place and operational right from the beginning suggests a design that is intelligent and purposeful.

The human cerebral cortex functions through a multitude of mechanisms, signaling pathways, and codes. To understand the depth of its irreducible complexity, it's crucial to discern the ways in which its various systems are interdependent and how they work in synchrony. Take, for instance, the regulatory codes that dictate when and how neurons fire. These codes, governed by a combination of genetic and epigenetic factors, determine the responses of neurons to various stimuli. Without the precise orchestration of these codes, the cerebral cortex would be a cacophony of unregulated activity. Simultaneously, these regulatory codes rely on intricate signaling pathways, which include neurotransmitters, ion channels, and various protein structures. If a signaling molecule isn't released correctly, the entire mechanism fails. This signaling mechanism, in turn, is dictated by manufacturing codes that ensure the right molecules are produced in the right places and at the right times. Furthermore, the cells in the cerebral cortex don't operate in isolation. They communicate with one another through a myriad of languages. For instance, neurotransmitters like dopamine or serotonin aren't merely chemicals; they're part of the brain's language. However, for these neurotransmitters to serve their function, there are receptor systems that need to understand this 'language.' Without the receptor, the neurotransmitter is like a key without a lock, pointless and non-functional. Additionally, consider the various feedback systems that allow cells to adjust their activity based on the output they produce. This dynamic adjustment process is fundamental for processes like learning and memory. A single misstep in this feedback mechanism could lead to erratic neural behavior. The system's ability to adjust and fine-tune its responses is based on another layer of communication and coding systems that monitor and regulate neural activity. Then there's the aspect of cellular maintenance and repair. The machinery that undertakes these processes, again governed by their own set of codes and languages, has to operate seamlessly with the cellular functions of the cerebral cortex. Any miscommunication could lead to neural degeneration. Given the above interdependences, suggesting that each of these systems could evolve step by step in isolation appears implausible. Without the complete system in place, the intermediate stages would not just be less efficient; they would be non-functional. It's akin to building a computer: having just the processor or just the memory wouldn't result in a functioning system. All the parts need to be present and perfectly integrated for the system to work.

The prefrontal cortex is associated with a suite of cognitive abilities known as executive functions, including complex problem-solving, advanced reasoning, planning, and decision-making. The significant expansion of this region in Homo sapiens relative to other primates is one of the hallmark anatomical differences between the species.  The prefrontal cortex (PFC) is a highly sophisticated region of the brain involved in a wide array of executive functions, and many molecular processes influence its development and function. The PFC is an intricately complex structure with many "codes" governing its function. These codes are both irreducibly complex and interdependent, meaning that no single code can be removed without affecting the overall function of the PFC. Just as a clock can't function properly if a single gear is removed, the PFC's operation is contingent upon each code's presence. For instance, the Epigenetic codes (like DNA Methylation and Histone Modification) shape gene expression, but without the Synaptic Code or the GPCR Code, the outcome of those expressions—neural communications—wouldn't function optimally. Each code, from the Acetylation to the Visual Code, contributes uniquely and indispensably to the PFC's ability to process information, regulate behavior, and support cognition. The seamless integration of these codes exemplifies their interdependence. For example, the DNA Repair/Damage Codes maintain genetic integrity, crucial for accurate gene expressions. These expressions, in turn, are influenced by the Genomic regulatory Code and translated into neural actions via codes like the GPCR and Endocytosis Codes. The Memory Code, reliant on accurate gene expression, synaptic function, and neurotransmission, underscores this interconnectedness. Therefore, to understand the PFC's behavior and cognitive outputs, one must appreciate the intricate ballet of these codes working in unison. To say that these codes work in isolation would be a gross misunderstanding of the intricate web of molecular, genetic, and neural interactions that the PFC orchestrates daily. The sheer number of codes and their diverse functionalities exemplify the multifaceted nature of the PFC and the brain at large. In the grand orchestra of the mind, each of these codes plays its indispensable note, creating the symphony of cognition, emotion, and behavior we attribute to the PFC. While not all of the codes listed are directly related to the PFC, several of them pertain to broader brain or cellular functions that indirectly influence the PFC. 

1. The Acetylation Code: Acetylation can influence the PFC's gene expression and synaptic plasticity.
2. The Allosteric Code: Influences neurotransmitter receptor function in the PFC.
3. The Axon Guidance Codes: Directs proper neural connections in the PFC during development.
4. The Bioelectric Code: Governs neural communication processes crucial for PFC function.
5. The Universal Brain Code: Relates to neural networks and cognitive processes in the PFC.
6. The Calcium Signaling Code: Central to neural excitability and plasticity in the PFC.
7. The Cell-Cell Communication Code: Mediates intricate signaling between neurons in the PFC.
8. The Cell Fate Determination Code: Dictates PFC neuron differentiation during development.
9. The Chromatin Code: Epigenetic changes in this code can impact PFC cognition and behavior.
10. The DNA Methylation Code: Epigenetic modifications influencing gene expression and function in the PFC.
11. The Code of Human Language: The PFC plays a role in higher-level language processing.
12. The Cytokine Codes: Neuroinflammation affecting the PFC can be influenced by immune signaling.
13. The Circadian Rhythm Codes: The PFC's cognitive performance fluctuates with circadian rhythms.
14. The Cytoskeleton Code: Affects neuronal structure and synaptic plasticity in the PFC.
15. The DNA Repair / Damage Codes: Maintains genomic integrity crucial for PFC cell function.
16. The DNA-Binding Code: Influences gene expression, impacting neuronal function in the PFC.
17. The Differentiation Code: Dictates the development and maturation of PFC neurons.
18. The Endocytosis Code: Critical for synaptic function in the PFC neurons.
19. The Endocrine Signalling Codes: Hormones can modulate PFC function.
20. The General Neural Codes: The PFC processes and integrates information from diverse neural sources to support cognition and executive function. It uses these neural codes to represent and manipulate information.
21. The Genomic Code: Genes and their expressions in the PFC can affect its structure and function, influencing behavior and cognition.
22. The Genomic regulatory Code: The non-coding regions of DNA in the PFC can regulate the expression of genes associated with cognitive processes.
23. The G-Protein Coupled Receptor (GPCR) Code: GPCRs are involved in many neurotransmission processes in the PFC, influencing activities such as mood regulation and decision-making.
24. The Growth Codes: These codes influence the development and maturation of the PFC, which continues to evolve into early adulthood.
25. The Histone Sub-Code: Epigenetic modifications in the PFC, including histone modifications, can affect gene expression, which in turn can influence cognition and behavior.
26. The Histone Variants Code: Variations in histone proteins in the PFC may be associated with diverse cognitive functions and susceptibilities to disorders.
27. The HOX Code Pattern Formation: While HOX genes mainly guide embryonic development, their patterns can influence the early formation of brain structures, including parts of the frontal lobe.
28. The Hypothalamic Code: The PFC and hypothalamus are interconnected and communicate, especially in the regulation of stress and emotion.
29. The Memory Code: The PFC plays a significant role in working memory, a type of short-term memory essential for tasks like problem-solving and planning.
30. The Metabolic Signaling Code: The metabolic processes within the PFC cells can influence their activity and function.
31. The Methylation Code: DNA methylation in the PFC can regulate gene expression, potentially impacting cognitive functions and susceptibility to mental disorders.
32. The Micro-RNA Codes: Micro-RNAs in the PFC can post-transcriptionally regulate gene expression, influencing neural processes and cognitive functions.
33. The Mnemonic codes: Mnemonic processes are integral to the PFC's role in memory formation, storage, and retrieval.
34. The Neuronal Activity-Dependent Gene Expression Code: Neuronal activity can influence gene expression in the PFC. When neurons fire, it can induce changes in gene expression that support synaptic plasticity, a fundamental mechanism for learning and memory.
35. The Neuronal Code for Reading: The PFC is involved in higher-order cognitive processes, which include understanding complex tasks like reading. Its interactions with other areas like the temporal lobe assist in processing and comprehending written material.
36. The Neuronal Hippocampal Codes: While the hippocampus is critical for forming new memories, the PFC plays a role in manipulating and using those memories, especially in tasks requiring working memory.
37. The Neural Perception & Recognition Codes: The PFC assists in processing sensory information, making sense of it, and using it in decision-making processes.
38. The Neural, Social Information Code: PFC is crucial in social cognition - understanding and predicting the behavior of oneself and others. It processes social cues and assists in navigating social scenarios.
39. The Neuronal Oscillatory /Frequency Codes: Neural oscillations in the PFC are associated with various cognitive functions. For instance, certain frequencies might be associated with attention or different stages of sleep.
40. The Methylation Code: DNA methylation can regulate gene expression in the PFC, influencing its structure, and function, and potentially impacting susceptibility to conditions like depression or ADHD.
41. The Neuropeptide Code: Neuropeptides in the PFC play roles in behavior, mood, and cognition. They can act as neurotransmitters or modulators.
42. The Nitric Oxide (NO) Signaling Code: Nitric oxide is a signaling molecule that can modulate neural activity. In the PFC, it may play roles in neural plasticity and memory.
43. The Nucleosome Code: The arrangement of nucleosomes can influence which genes are accessible to be read and transcribed. In the PFC, this could influence the expression of genes crucial for its functions.
44. The Olfactory Code: While primary olfaction processing occurs in the olfactory bulb and other regions, the PFC can be involved in higher-order processing, especially if an olfactory stimulus requires a decision or triggers a memory.
45. The Phosphorylation Code: Protein phosphorylation can modify the activity of proteins within neurons. In the PFC, this could affect neuron signaling, synaptic plasticity, and thus cognitive functions.
46. The Neuronal Activity-Dependent Gene Expression Code: This code describes the interplay between electrical activity in neurons and gene expression. In the PFC, such activity-dependent gene expressions can influence cognitive and emotional processing.
47. The Neuronal Code for Reading: Since the PFC plays a role in higher cognitive functions, it is involved in complex tasks like reading comprehension and semantic processing.
48. The Neural Perception & Recognition Codes: The PFC is integral in interpreting and recognizing sensory information, especially in the context of decision-making or assessing the relevance of sensory inputs.
49. The Neuronal Oscillatory /Frequency Codes: Neural oscillations in the PFC, such as gamma or theta waves, are linked to various cognitive tasks, including attention, memory, and decision-making.
50. The Serotonin Code: The neurotransmitter serotonin significantly impacts mood and behavior, and its signaling pathways are active in the PFC, affecting emotional regulation and executive functions.
51. The Synaptic Code: Synaptic transmission in the PFC is central to information processing, learning, and memory.
52. The Protein Phosphorylation Code: Protein phosphorylation events in the PFC can modulate neural signaling and influence behaviors like learning and memory.
53. The RNA Code: RNA molecules, including coding and non-coding roles, in the PFC play crucial roles in gene expression, neural plasticity, and cognition.
54. The RNA Editing Code: Post-transcriptional modifications in the PFC can have implications for neuronal function and plasticity.
55. The Transcription Factor Binding Code: Transcription factors in the PFC regulate gene expression patterns critical for cognitive processes and neural plasticity.
56. The Ubiquitin Code: The process of ubiquitination in the PFC is involved in synaptic plasticity, learning, and memory.
57. The Thermal / Temperature Neuronal Codes: The PFC might process temperature-related information as it pertains to decision-making or assessing environmental relevance.
58. The Translational Control Code: This code, active in the PFC, is crucial for regulating protein synthesis associated with synaptic plasticity and memory.
59. The Tissue Code: The PFC, like other brain regions, is made up of a specific arrangement of cells and structures, each with its molecular characteristics. This tissue-specific code is crucial for the PFC's distinct functions.
60. The Tissue Memory Code: While the PFC does not store memories in the way that the hippocampus does, it is involved in the processing and utilization of memories for decision-making and behavior regulation.
61. The Tissue spatial code: The spatial arrangement of neurons and their connections in the PFC can affect its functions. For example, distinct areas of the PFC have specialized roles, and the connections between these areas create a network that supports higher-order cognition.
62. The Tubulin Code: Microtubules, made of tubulin proteins, are crucial components of neurons. Modifications and interactions in the tubulin code could influence neuron morphology, intracellular transport, and even signal transduction in the PFC.
63. The Visual Code: While the primary visual processing occurs in the occipital lobe, the PFC plays a role in higher-order visual processing, such as interpreting and making decisions based on visual information.
64. The Perception Code: The PFC is integral in processing and interpreting various sensory perceptions. It doesn't only process the raw sensory input but also combines this information with internal states, past experiences, and other relevant data to produce an integrated perception.

Many of the mentioned "codes" or processes can interact or influence one another, their interactions are biochemical, electrical, and physical processes that lead to changes in cellular or tissue behaviors. These processes crosstalk in the context of the PFC:

1. The Acetylation Code & The Chromatin Code: Within the PFC, epigenetic modifications like histone acetylation can influence the expression of genes associated with higher cognitive functions. The acetylation of histones in the PFC can directly impact cognitive processes like decision-making, working memory, and emotional regulation.
Language: Epigenetic signaling and molecular recognition between DNA-binding proteins and DNA motifs.
2. The Memory Code & The Neuronal Activity-Dependent Gene Expression Code: The PFC plays a pivotal role in working memory. When tasks activate the PFC, specific patterns of neurons fire. This activity can induce changes in gene expression critical for synaptic plasticity within the PFC, further reinforcing memory processes.
Language: Neural firing patterns and intracellular signaling cascades that influence gene transcription.
3. The Calcium Signaling Code & The Bioelectric Code: In PFC neurons, calcium signaling is crucial for synaptic plasticity. Calcium influx during neuronal activity in the PFC plays a role in modulating the strength of synaptic connections, affecting cognitive functions like decision-making and problem-solving.
Language: Electrochemical gradients and intracellular calcium-mediated signaling pathways.
4. The Ubiquitin Code & The Synaptic Code: The synaptic strengths in the PFC, vital for cognition and executive functions, can be modulated by the ubiquitination of certain synaptic proteins, influencing synaptic plasticity.
Language: Post-translational protein modifications and synaptic transmission dynamics.
5. The Micro-RNA Codes & The RNA Code: Micro-RNAs in the PFC can target specific messenger RNAs, influencing protein synthesis related to neural processes like synaptic plasticity, learning, and memory.
Language: RNA-RNA interactions and translation control mechanisms.
6. The Neuronal Code for Reading & The Code of Human Language: The PFC is involved in the integration and processing of linguistic information. During reading, the PFC may be engaged in comprehension, especially in tasks requiring semantic processing or executive control over linguistic input.
Language: Neural firing patterns associated with linguistic processing and comprehension.
7. The Neural, Social Information Code & The Neuronal Hippocampal Codes: The PFC's role in social cognition often requires integration with memories from the hippocampus, making these codes interdependent when processing complex social scenarios.
Language: Neural firing patterns and network synchrony between different brain regions.
8. The Neuronal Oscillatory/Frequency Codes & The Memory Code: In the PFC, distinct neural oscillations are correlated with stages of working memory processing, including encoding, maintenance, and retrieval.
Language: Oscillatory neural activity and its synchronization across neural networks.

When observing the human prefrontal cortex (PFC), its intricate architecture is an awe-inspiring connectivity and functionality. This complexity not only arises from the sheer number of neurons but also from the multifaceted signaling systems, codes, and regulatory languages that govern its functions. Each of these elements is integral for the PFC to operate efficiently. Without one, the entire system could falter. Consider the interplay between the molecular signaling pathways and the neural codes they activate; without a coherent language or code system, the signaling pathways wouldn't effectively regulate neural activity. Neural proteins are coded by specific sequences in the DNA, but their expression, transport, and function in the PFC require a myriad of other molecules and codes. The transcription factors, the molecular chaperones, the synaptic receptors – each has a unique language, yet all must "speak" to each other in perfect synchrony for normal cellular function. If one of these systems were to evolve in isolation, without the concurrent evolution of its complementary systems, it would serve no purpose and would likely be discarded in the evolutionary process. Given this profound interdependence, the idea of incremental evolution of the PFC becomes a complex issue. An evolutionary path that produces an intermediate or partially functional PFC might be rendered non-functional due to the lack of interconnected systems. It's akin to developing a cutting-edge computer chip but not having the appropriate software to run it, or vice versa. The chip, no matter how advanced, would be rendered useless. The seamless crosstalk between various cellular components and languages in the PFC further accentuates this complexity. Signaling pathways communicate with genetic codes to regulate protein expression, which in turn influences neuronal activity. This synchronized dance ensures the PFC's optimal functioning. Any disruption in this crosstalk, such as a miscommunication or a failure in one of the systems, would jeopardize the entire operation.

The PFC, as a part of the human brain, has undergone remarkable evolutionary developments, leading to the emergence of novel functions and capabilities. 

 Complex Planning and Decision Making: One of the most distinct capabilities of the human PFC is its role in advanced planning and decision-making processes. This involves not only weighing immediate outcomes but also considering long-term consequences, evaluating risks and rewards, and making decisions that are aligned with our goals and values. This goes beyond the simpler cause-and-effect thinking seen in many other species.
 Abstract Thought and Symbolic Reasoning: Humans have the ability to think abstractly, reason symbolically, and understand complex concepts that are not immediately present or tangible. The PFC allows us to ponder philosophical questions, understand metaphors, and appreciate art and literature, which are manifestations of our abstract thinking capabilities.
 Self-awareness and Reflection: While many animals show signs of self-recognition, the depth of self-awareness and introspective reflection in humans is unparalleled. The PFC enables us to have a deep understanding of ourselves, our motivations, and our place in the world.
 Regulation of Emotions and Impulses: While emotions are generated in more primitive parts of the brain, the PFC plays a crucial role in regulating these emotions. It allows us to respond rationally to emotional stimuli, control our impulses, and act in socially acceptable ways.
 Working Memory and Task Management: The PFC is instrumental in our working memory, which allows us to hold and manipulate information in our minds over short periods. This ability is crucial for tasks like problem-solving, mental arithmetic, and complex reasoning.
 Moral Reasoning and Empathy: The human sense of morality and our ability to empathize with others, even those outside our immediate social or cultural group, is a testament to the PFC's advanced functions. This has shaped our social structures, ethical codes, and societal norms.
 Adaptability and Learning: The PFC plays a key role in our ability to learn from our experiences, adapt to new situations, and adjust our behaviors based on feedback. This adaptability has been crucial for human survival and progress.

The functional emergence in the human prefrontal cortex goes far beyond mere size enhancement. It's about the development of intricate, interrelated capabilities that underpin our most advanced cognitive functions. The complexity of these functions and their interconnectedness poses intriguing questions about the feasibility of incremental evolutionary processes that would have led to their emergence.

The Prefrontal Cortex: An Energy Powerhouse

The human prefrontal cortex stands as an unmatched marvel in the realm of neuroanatomy. Its complexity and size surpass that of any other species, rendering it a pivotal driver of our advanced cognitive abilities, from abstract thinking to planning and decision-making. But with this unparalleled complexity comes an insatiable energy demand. The PFC consumes a significant proportion of the body's energy, especially when we consider its relative size to the rest of the brain. It becomes an enigma then: How could such an energy-demanding structure have emerged through incremental evolutionary steps? For the PFC to evolve, not only would anatomical changes have been essential, but also systemic adaptations throughout the organism to cater to its high-energy needs. This encompasses a wide range of changes, from the molecular level, with specific proteins and enzymes, to the organismal level, including alterations in diet and metabolism. The synchronicity and coordination required for these changes present a challenge to a stepwise evolutionary model. One might argue that every intermediate stage of the PFC's development would demand corresponding systemic adaptations. Each of these stages would need to offer some survival or reproductive advantage to be preserved and refined over generations. But given the intricate balance between the energy input and output required for the PFC's function, it's challenging to identify what these intermediate advantages might be. This puzzle highlights potential shortcomings in the traditional evolutionary narrative and lends weight to the notion that such a system, in its entirety, may hint at design rather than chance and incremental changes.

Genomic Difference: The Implications of 1-2%

On the surface, a 1-2% difference between humans and chimpanzees seems minimal. However, when delving into the intricacies of genetics, this seemingly slight distinction takes on a profound significance. Given the vastness of the human genome, which consists of roughly 3 billion base pairs, a difference of even 1% amounts to a staggering 30 million base pair differences. This number is not trivial. To put it into perspective, if we were to read out these differences at a rate of one base per second, it would take almost a year to go through them all. It's crucial to understand that it's not just the quantity of differences but the quality or the functional implications of these differences that matter. Some genetic changes can lead to significant physiological, anatomical, and functional disparities between species. For instance, differences in gene regulation, which might only involve a handful of base pairs, can lead to vast differences in gene expression patterns, influencing developmental pathways and leading to distinct phenotypic outcomes.

The studies,  specifically those by Shiho Endo 1, and Gennadi V. Glinsky 2 , represent significant advances in our understanding of human-specific regulatory sequences and proteins, respectively. These findings are profound as they challenge the established idea of common ancestry between humans and apes, a cornerstone of evolutionary biology. 

Human-Specific Regulatory Sequences: Glinsky's work uncovers that human-specific regulatory networks play pivotal roles in crucial biological processes, from embryonic stages to adult brain development. Such specificity, not found in other primates, is evidence that humans have regulatory mechanisms entirely distinct from those in our closest primate relatives. When we consider the vast number of de novo HSRS (human-specific regulatory sequences) Glinsky mentions, it's evident that these aren't minor deviations but rather substantial changes that can't be explained merely by shared common ancestry.
Unique Human Proteins: Endo's research illuminates the presence of proteins, like FAM75, that are unique to humans. The fact that such a protein arose due to a single nucleotide polymorphism and yet plays a potential role in vital processes like sperm development and fertilization is intriguing. This suggests that there were specific and possibly guided changes in the human genome, leading to unique functionalities. The existence of exclusive human genes and proteins defies the idea that humans and apes merely have regulatory differences.
Genome Comparisons and Their Limitations: While DNA sequence comparisons between humans and chimpanzees show minor nucleotide differences, the emphasis on aligned sequences potentially ignores significant genomic regions that account for the pronounced differences between the two species. And, as highlighted, methods that depend on sequence alignment might overlook short sequences that don't have longer similarities. Such sequences, previously dismissed as noise, hold the key to understanding some profound differences between species.
Brain Evolution and Uniqueness: The remarkable expansion and intricacies of the human brain, as mentioned in Mainá Bitar's work, remain one of the most profound distinctions between humans and other primates. While the genetic underpinnings of this expansion are yet to be fully understood, it's evident that simple shared ancestry might not account for these significant changes.

Complexity Beyond Base Pairs

It's not just about the base pairs themselves. The interaction of genes, their regulatory elements, and the proteins they encode creates a web of complexity. A single mutation in a regulatory element, for example, can have cascading effects, altering the expression of numerous genes downstream. The myriad differences and the nuanced interactions between genes underscore the challenges in explaining the divergence of humans from our primate relatives. While evolutionary mechanisms can account for some changes, the sheer complexity and coordination seen in human-specific traits, driven in part by these 30 million base pair differences, hint at a system that seems intricately designed rather than a product of random, incremental alterations.

The Ripple Effect of Functional Genes

When discussing genetics, there's an inclination to focus on the raw data—the sheer number of genes, the sequence of base pairs, and the percentage differences. However, the real story, and perhaps the most fascinating aspect of genetics, is not in the numbers but in the functional impact of these genes. It's the quality, the nuances, and the interactions that truly shape an organism. Regulatory genes act as the puppeteers of the genome. They don't just serve a solitary function; they control the activity of other genes, determining when, where, and how those genes are expressed. This regulatory system is akin to a sophisticated orchestration where a single conductor can influence the entire symphony. A minor change in these genes can be likened to a change in the conductor's instructions, leading to a drastically different performance. When regulatory genes are altered, the cascading effects on development can be profound. For instance, a single mutation in a regulatory gene during embryonic development could divert the trajectory of tissue formation, leading to entirely new structures or significantly altered existing ones. These are not just surface changes but can redefine the very blueprint of an organism. But the influence of these genes doesn't stop at anatomy. By dictating the activity of other genes, regulatory genes can impact physiological processes, metabolic pathways, and even behaviors. A subtle change in the regulatory system can, for example, modify neural pathways in the brain, leading to advanced cognitive capabilities or novel behaviors. It's also essential to recognize that the genome is not a static entity. Genes, especially regulatory genes, interact in a dynamic network. They respond to environmental cues, internal signals, and feedback from other genes. This creates a multi-layered, intricate system where each gene can potentially influence, and be influenced by, numerous others. This makes predicting the outcomes of genetic changes incredibly challenging, as a single alteration can set off a chain reaction of events. The importance of functional genes, particularly regulatory genes, cannot be understated. They exemplify how the genome is more than just a collection of genetic codes; it's a dynamic, interconnected system where quality, in terms of function and impact, often outweighs quantity.

"Junk" DNA: A Misnomer in Genomic Understanding

Historically, the non-coding regions of DNA were labeled as "junk" due to a lack of understanding of their function. These sequences, which don't code for proteins, make up a significant portion of our genome. However, as genomic science has progressed, it's become evident that these regions are far from being redundant or without purpose. A substantial part of non-coding DNA functions as regulatory elements. These sequences can act as switches, turning genes on or off, or modulating the degree to which they're active. By governing gene expression, these elements have profound impacts on every facet of an organism's biology, from development to daily function. For instance, certain non-coding elements can determine when a gene gets activated during brain development, influencing the formation of neural circuits. Some non-coding regions play essential roles in maintaining the structure and integrity of the chromosome. For example, telomeres—repetitive sequences at the ends of chromosomes—prevent chromosomes from fraying or sticking to each other. Centromeres, another non-coding region, help in the proper segregation of chromosomes during cell division. Many segments of "junk" DNA are remnants of ancient viruses or other mobile genetic elements. Over time, some of these sequences have been co-opted and repurposed by the host genome. They provide a unique insight into our evolutionary history and demonstrate nature's ability to reuse and repurpose genetic material in innovative ways. Recent studies have underscored the importance of non-coding DNA in brain function. Some of these regions are actively transcribed into non-coding RNAs, which play crucial roles in neural plasticity, memory formation, and neuroprotection. Additionally, alterations or mutations in certain non-coding regions have been associated with neurological disorders, emphasizing their critical role in maintaining brain health. The term "junk" DNA may have been a product of its time, reflecting the limited understanding of genomics in earlier years. Today, it's clear that these non-coding regions hold secrets to complex regulatory networks, evolutionary histories, and crucial biological functions. The deeper we delve into the genome, the more we recognize the intricate ballet of coding and non-coding sequences working in harmony to orchestrate the vast complexity of life.

Decoding the Genetic Labyrinth

The journey of unraveling the mysteries of life has brought science to the doorstep of our very genetic essence. The genetic distinction between humans and chimps, although quantitatively small, has profound qualitative implications. With around 30 million base pair differences, the divergence is not just about individual genes but about the entire orchestration of cellular processes. The molecular dance within cells is a marvel of coordination and precision. Processes like DNA replication, protein synthesis, and cellular signaling are marvelously intertwined. It's a system where each component often relies on several others to function correctly. A disruption in one part can cascade throughout the system, possibly leading to dysfunction or even collapse. Evolutionary biology posits that complex systems arise incrementally, through a series of small, beneficial changes that are preserved through natural selection. Yet, when one considers the sheer complexity and interdependence of biological systems, a question emerges: How could these systems, which seem to require multiple parts to be present and functional simultaneously, arise piecemeal over time? Would not an incomplete or partially formed system be non-functional and thus offer no selective advantage? While evolution tries to explain the transition from ape to human as a result of gradual genetic changes accumulating over millions of years, the clear genetic and functional distinctions between the two species are thought-provoking. A mere 1-2% difference in DNA has led to disparities in cognitive abilities, emotional depth, social structures, and even artistic expression. How could such monumental differences in function and capability arise from what seems to be a relatively small genetic gap?  The aforementioned complexities, especially the apparent interdependence of molecular systems, lend themselves to the argument that such systems might have been intentionally designed. If true, this would mean they were instantiated in their entirety, rather than emerging gradually.
Evolution, while a robust theory in many respects, grapples with explaining the rapid emergence of high complexity. The fossil record, for example, sometimes showcases sudden appearances of new forms rather than the expected gradual transitions. Additionally, the intricate coordination and mutual dependencies observed in biological systems pose challenges to the traditional model of incremental evolutionary development. Whether through the lens of evolution or intelligent design, the journey of understanding remains a testament to the profound intricacies of life.

1. Shiho Endo, Kenta Motomura, Masakazu Tsuhako, Yuki Kakazu, Morikazu Nakamura, & Joji M. Otaki (2019). Search for Human-Specific Proteins Based on Availability Scores of Short Constituent Sequences: Identification of a WRWSH Protein in Human Testis. Link.
2. Gennadi V. Glinsky (2020). A Catalogue of 59,732 Human-Specific Regulatory Sequences Reveals Unique-to-Human Regulatory Patterns Associated with Virus-Interacting Proteins, Pluripotency, and Brain Development. Link.
Mainá Bitar (2019). Genes with human-specific features are primarily involved with brain, immune, and metabolic evolution. Link.



Last edited by Otangelo on Thu Sep 28, 2023 1:35 pm; edited 4 times in total

https://reasonandscience.catsboard.com

19Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sun Sep 17, 2023 3:12 pm

Otangelo


Admin

2. Brain Connectivity

The human brain stands as one of the pinnacles of biological complexity. Its intricate web of dendritic spines, synaptic connections, and neural circuits underpins our advanced cognitive abilities. While our primate cousins, such as the chimpanzee, also boast intricate brain connections, the qualitative and quantitative differences in our neuroanatomy are evident. The density, pattern, and organization of human neural connections contribute to our exceptional capacity for abstract thought, self-awareness, language, and more. The human brain's architecture is not only unique but also remarkably efficient. Weighing approximately three pounds, it comprises nearly 86 billion neurons, with each neuron forming thousands of synaptic connections to other neurons. This results in a complex network with trillions of synapses, ensuring rapid and diverse communication pathways. The dendritic spines, which are tiny protrusions emanating from the dendrites of neurons, play a pivotal role in transmitting electrical signals. Their dynamic nature, where they can grow, retract, and modify their shapes, allows for plasticity, the brain's ability to adapt and rewire itself based on experiences. Such plasticity is a cornerstone of learning and memory formation. The cerebral cortex, the outermost layer of the brain responsible for many higher-order functions, is notably convoluted in humans. The folds (gyri) and grooves (sulci) increase the surface area, allowing for more neurons to be packed into this region. The complexity and depth of these folds are more pronounced in humans than in any other primate. Furthermore, specific regions of the human brain have undergone notable expansion and specialization. The Broca's and Wernicke's areas, integral for speech production and comprehension respectively, are highly developed in humans, underscoring our unparalleled linguistic capabilities. The prefrontal cortex, involved in abstract thinking, planning, decision-making, and social interactions, is another region that's disproportionately large in humans. Its extensive connections to other brain regions enable us to reflect on the past, plan for the future, and engage in profound philosophical and moral reasoning. While chimpanzees and other primates exhibit remarkable cognitive abilities and display a degree of neural complexity, the human brain's specialization enables a spectrum of cognitive, emotional, and creative capacities that remain unmatched.  From the lens of evolutionary biology, the development of such a sophisticated neural network is explained through gradual adaptations that provided selective advantages. However, the nuanced differences and the sheer complexity seen in the human brain, down to the molecular and cellular level, poses questions. How do minor, incremental changes, over time, culminate into a system of such profound capability and complexity? When considering the interdependence of biological systems, the intricate codes, signaling pathways, and proteins that seem to have been operational from their inception, this points towards a designer. . The profound leap from ape-like neural systems to the human brain's intricacy seems too vast to bridge through mere evolutionary incremental changes alone. The traditional evolutionary model rests on the idea of slow, gradual changes accumulating over vast stretches of time. Yet, certain biological systems, especially ones as complex as the human brain, challenge this model. Can a series of small, beneficial mutations truly account for the vast neural differences that separate us from our primate relatives? Whether viewed through the lens of evolution or intelligent design, the quest to understand the origins of our neural marvels remains one of the greatest scientific and philosophical endeavors.

Chimps, our brothers ?  1411

3. Gyrification

Gyri (singular: gyrus) and sulci (singular: sulcus) are features of the brain's surface anatomy and are critical to understanding the brain's organization and structure. Gyri (Gyrus) are the raised, convoluted ridges that you see on the surface of the brain. They increase the surface area of the cerebral cortex, allowing for more neurons to be packed into the space available inside the skull. This increased neural density is thought to play a significant role in the advanced cognitive abilities of humans. Sulci (Sulcus)are the grooves or depressions between the gyri. Just like gyri, sulci also contribute to increasing the overall surface area of the brain. Some sulci are quite deep and are sometimes called "fissures." A prominent example is the "Sylvian fissure" (or lateral sulcus), which separates the temporal lobe from the frontal and parietal lobes. The presence of numerous gyri and sulci gives the human brain its characteristic folded appearance. The pattern and depth of these structures can vary among individuals but are generally consistent enough to allow neuroanatomists to identify specific gyri and sulci across different human brains. The extensive gyrification (folding) of the human brain is one of the features that distinguishes our brains from those of many other mammals, including some primates, and is thought to be related to our advanced cognitive abilities. The gyri and sulci, enhancing our cerebral cortex's surface area, underpin our advanced cognitive capacities. This distinction invites consideration about the feasibility of incremental evolutionary steps leading to such complexity.  The human cerebral cortex, adorned with its elaborate gyri and sulci, showcases an architecture optimized for enhanced cognitive processing. These intricate folds provide a significantly expanded surface area, enabling more neural real estate within the confines of the human skull. Such a design is not merely about housing more neurons but about facilitating complex neural networks that support abstract thought, reasoning, creativity, and advanced linguistic abilities. By contrast, the less gyrified brain of a chimp, while impressive in its own right, does not possess the same degree of architectural sophistication. How such pronounced differences emerged, especially if premised on the idea of small, gradual changes, presents a significant challenge for evolutionary theory. At a molecular and cellular level, the operation of the human brain—and indeed all biological systems—relies on a vast array of codes, signaling pathways, and proteins. These systems display remarkable interdependence; the failure or absence of one component can compromise the entire mechanism. Considering the transition from ape to human, it's not just about structural changes in the brain, but how these changes dovetail with myriad other molecular and cellular adaptations. The clear genetic and functional distinctions between humans and apes, coupled with the intricate web of interdependencies in our biological systems, pose questions. Could such a meticulously coordinated system truly be the product of incremental changes? Or does it hint at a design that's more deliberate, echoing the sentiments of those favoring intelligent design? It's worth noting that while evolutionary biology posits mechanisms through which incremental changes can accumulate over vast timescales, leading to profound adaptations, the sheer complexity and interdependence of the human brain remain points of fascination and debate.

4. Language Centers

One of the most striking distinctions between human brains and those of our closest primate relatives is the pronounced development and specialization of regions like Broca's and Wernicke's areas. These regions, intricately tied to speech production and language comprehension, underscore the unparalleled complexity of human communication and abstract thought. While chimps and other primates exhibit regions analogous to these areas, they do not possess the same degree of development or specialization, making them less equipped for intricate language-based communication. This profound neuroanatomical distinction challenges the notion of a simple, gradual evolutionary progression. How can mere incremental changes account for the vast gulf in cognitive and communicative abilities between humans and chimps? The molecular and cellular intricacy of biological systems, paired with sophisticated codes, signaling pathways, and proteins, seems to be in stark contrast with the concept of incremental evolution. This complexity becomes especially perplexing when considering the transition from ape to human. The leap is not just in genetic terms but is glaringly evident in functional capacities. How could a series of random mutations and selections account for the emergence of intricate brain structures dedicated solely to language and communication? Some argue that such profound differences, especially when considering the clear genetic and functional distinctions, point towards a design or a purpose beyond mere chance. While evolutionary biology provides explanations rooted in natural selection and adaptation, some aspects of the human experience and anatomy seem to stretch the boundaries of what can be expected from gradual evolutionary processes alone.

Chimps, our brothers ?  Speech10

Human speech is a symphony of intricately interwoven components, seamlessly blending the physical and cognitive domains. To shed light on this sophisticated system, let's delve into the crucial facets of speech production and comprehension:

Consciousness and Language: The grounding of consciousness and memory within our physical being is uniquely profound. Speech, drawing upon these depths, forms a bridge to the nuanced world of language, differentiating itself from physical attributes like mass or charge.
Language Tiers: Just as a building rises from its foundation to its pinnacle, language escalates in complexity. Beginning with rudimentary vocal sounds, it evolves into spoken words, builds into sentences, and eventually takes the form of intricate texts. This progression isn't a mere addition but rather a metamorphosis: words emerge from vocal sounds, sentences from grammatical words, and text from structured sentences. It's an interconnected hierarchy, where each level sets the stage for the next.
The Orchestra of Voice Production:
Vocal Generation: It begins with the lungs, supplying the air. This air stirs the vocal folds in the larynx into vibration, crafting sound. This sound is then shaped by resonators like the throat and nasal passages, crafting our distinctive voice.
Articulation: The sound, once produced, is sculpted into discernible speech through the dance of articulators like the tongue, soft palate, and lips.
Voice's Tripartite System:
Breath Dynamics: Fueled by the diaphragm, chest muscles, and lungs, this system ensures that air pressure is just right for vocal vibrations.
The Sound Forge: The larynx and vocal folds work in harmony, converting air pressure into the rudimentary sounds of speech.
The Refinement Workshop: The throat, mouth, and nasal cavities fine-tune this basic sound into discernible speech.
Larynx - The Maestro: Situated at the heart of voice production, the larynx is home to structures pivotal for modulating speech. As they interact and adjust, the resultant vocal nuances give depth to our speech. The glottis, or the gap between vocal folds, is central to this modulation.
Supporting Cast: Our lungs, akin to bellows, infuse the required energy into speech. The nervous system choreographs this ensemble, linking it to the brain's motor cortex. This ensures harmony as facial, oral, and throat muscles move to shape speech. Nerves such as the Trigeminal and Facial act as the unsung backstage crew supporting this performance.
Brain - The Grand Conductor: Speech comprehension and production find their maestro in the human brain. Sound waves, once they reach our ears, undergo processing in the auditory cortex. The brain, like a masterful conductor, employs various sections, from the angular gyrus to Wernicke’s area, orchestrating them to decode these sounds into meaningful language. The pathways connecting auditory and frontal lobes facilitate the delicate dance between sound recognition and speech articulation.
Neurological Choreography: Regions like Broca’s and Wernicke’s areas, along with others like the temporal pole, each play their part in the intricate ballet of language processing.
Modern research champions the idea of a distributed choir for language processing, refuting the older soloist model.
Emotion - The Soulful Undertones: The richness of human emotions, ranging from joy to anxiety, adds layers of depth to speech, much like an undercurrent that gives a river its pull.
Speech Production's Symphony: Breathing sets the rhythm, sound production provides the melody, resonance adds the harmony, and articulation delivers the final notes, culminating in the masterpiece that is human speech.

Philosophical Musings: If speech is a symphony, it's one where every note depends on the other. The whole process is so interconnected that a missing piece disrupts the entire performance. It challenges the conventional wisdom of evolutionary processes that would suggest a step-by-step assembly. This leads to a contemplative question: Was the human ability to communicate, with its intricate design, intended rather than accidental?

5. Brain Chemistry 

The chemical composition of the human brain plays a critical role in supporting the remarkable cognitive abilities, emotional complexity, and intricate social interactions that distinguish us from other primates, including chimpanzees. While both humans and chimps share some similarities in brain structure and neurotransmitter systems, there are notable differences that underlie our distinct cognitive and emotional capacities. Dopamine is a neurotransmitter associated with reward, motivation, and reinforcement learning. In humans, the dopamine system is more developed and intricate than in chimpanzees. This heightened dopamine system in humans may contribute to our ability to set long-term goals, plan, and pursue complex objectives. Serotonin is involved in regulating mood, social behavior, and emotional well-being. Variations in serotonin levels and receptor distribution can influence mood disorders such as depression and anxiety. The unique serotonin system in humans likely contributes to our range of emotional experiences and ability to form complex social bonds. Glutamate is the primary excitatory neurotransmitter in the brain and is crucial for cognitive functions like memory, learning, and synaptic plasticity. Humans have a more sophisticated glutamate system, enabling us to process and store vast amounts of information, leading to advanced cognitive abilities. Humans have a disproportionately larger prefrontal cortex compared to other primates. This region is associated with executive functions such as decision-making, problem-solving, and self-control. The expanded prefrontal cortex contributes to our capacity for complex reasoning and planning. The neocortex, particularly the association areas, is significantly more developed in humans. This part of the brain is responsible for higher-order cognitive functions, including language, abstract thinking, and social cognition. The neocortex's expansion in humans is closely tied to our advanced cognitive abilities. Humans have a well-developed "theory of mind," which refers to the ability to understand and attribute mental states, beliefs, intentions, and emotions to oneself and others. This cognitive skill is essential for complex social interactions, empathy, and cooperation. Our brain's unique neurochemical makeup and connectivity support a higher capacity for empathy, allowing us to connect emotionally with others, understand their perspectives, and engage in prosocial behaviors. The intricate interplay of neurotransmitters and neuromodulators in the human brain contributes to our broad spectrum of emotions, ranging from love and compassion to jealousy and guilt. This emotional depth enriches our social interactions and relationships. Broca's Area and Wernicke's Area are specialized regions in the human brain that are crucial for language processing and production. While primates like chimps have basic communication abilities, the human brain's unique neural circuitry allows for the complex structure and syntax found in human language. The differences in the chemical composition, neuroanatomy, and neural circuitry of the human brain compared to chimpanzees contribute to our advanced cognitive functions, emotional depth, and complex social interactions. These adaptations have enabled humans to develop complex societies, cultures, and the ability to communicate and cooperate on a scale unparalleled in the animal kingdom. Our brain's unique features are a testament to the evolution of human cognition and behavior.

6. Growth and Development

Extended Childhood in Humans: Humans have an unusually long childhood and adolescence compared to other species. This prolonged developmental period is closely tied to our brain's growth patterns. The human brain continues to develop and rewire itself well into our twenties. This extended period of neuroplasticity, or the brain's ability to change and adapt, plays a vital role in our cognitive, emotional, and social development. The slow maturation allows humans to be incredibly adaptable. We're not just learning basic survival skills; we're also absorbing cultural norms, languages, social cues, and a plethora of knowledge that aids in our survival and success in varying environments. An extended childhood also means that human offspring are dependent on caregivers for longer. This has led to the development of intricate social structures and familial bonds that provide the necessary support for these prolonged developmental periods.
Chimpanzee Development: While chimpanzees share about 98-99% of their DNA with humans, their developmental timelines are starkly different. Chimp brains experience rapid growth shortly after birth but reach their full size much sooner than human brains. By the age of five, a chimp's brain is nearly fully grown. With a shorter childhood, chimps must quickly acquire essential survival skills. They rapidly learn to find food, navigate their arboreal environment, and understand the basics of their troop's social hierarchy. Though shorter, chimps do have a period of learning where they pick up certain behaviors and tools usage passed down in their group. However, this cultural transmission is limited compared to the extensive cultural knowledge passed down among humans.

The extended developmental period in humans supports the growth of our advanced cognitive abilities. Our capacities for abstract thought, problem-solving, language, and planning are unparalleled in the animal kingdom. Humans can accumulate knowledge across generations, leading to cultural evolution. Over generations, humans have built upon past knowledge, leading to advancements in technology, art, science, and more. Chimps, while they have cultural behaviors, don't exhibit this level of cumulative cultural evolution. Our extended childhood and adolescence also support the development of complex emotional and social behaviors. Humans have intricate social networks, deep emotional bonds, and an ability to cooperate with large groups of non-kin individuals. The differences in brain development timelines between humans and chimps have significant implications for the cognitive, social, and cultural complexities of each species. The slow and sustained growth of the human brain, coupled with our extended childhood, plays a crucial role in shaping who we are as a species.

7. Brain-to-Body Ratio

The brain-to-body ratio, also known as the encephalization quotient (EQ), has been a topic of interest to many researchers trying to understand the evolution of intelligence and cognitive capacities in various species.  The brain is an energy-intensive organ. In humans, it represents about 2% of the body's weight but consumes approximately 20% of the body's energy. This disproportionate energy consumption supports advanced cognitive functions and capabilities. The evolutionary enlargement of the human brain required metabolic trade-offs. Some theories suggest that our digestive system became more efficient, or energy was diverted from other systems, to support our larger brains. A larger brain, especially the expansion of the neocortex in humans, allows for enhanced cognitive capabilities. This includes advanced problem-solving, abstract thinking, planning, and introspection. The human brain's size and structure support intricate language skills, both in terms of understanding and production. It's not just about the number of words we can use, but the depth of concepts, emotions, and abstract thoughts we can convey and understand. Humans have intricate social structures and can maintain stable relationships with a vast number of individuals. This capability is often linked to the "social brain hypothesis," which proposes that the complexity of primate social interactions, especially in humans, is a significant driver for brain enlargement. While chimps and some other animals use tools, humans have taken tool-making to unparalleled levels. Our brains allow us to visualize, plan, and create tools of increasing complexity, which has been pivotal in our species' survival and dominance. With a larger brain-to-body ratio, humans have the capacity for cumulative culture. This means that we don't just learn and pass on knowledge; we build upon it, leading to the rapid advancement of technology, arts, sciences, and societal structures. Our large brains have enabled us to adapt to various environments worldwide, from the cold Arctic tundras to the hot deserts. We can plan, innovate, and modify our surroundings in ways that no other species can. As discussed earlier, a larger brain requires a prolonged developmental period. This means human offspring are vulnerable for longer and depend on caregivers for extended periods. The complexity of the human brain also means there's more that can go awry. Humans are susceptible to a range of neurological and psychological disorders.
The larger brain-to-body ratio in humans compared to chimps signifies more than just size. It's a testament to the cognitive, social, and cultural intricacies that define us as a species. It underscores the balance between the benefits of advanced cognitive capabilities and the energy demands and vulnerabilities that come with them. Why would evolution lead to a brain so advanced that it contemplates the universe, arts, philosophy, and its own existence? Many of our brain's capabilities go beyond what's strictly necessary for survival.

8. Functional Specialization

Certainly, functional specialization refers to the dedication of specific regions of the brain to specific tasks or functions. This specialization allows for efficient and rapid processing in these dedicated regions. Let's delve deeper into this topic with respect to both humans and chimps: As both humans and primates evolved, so did the need for rapid and efficient processing in certain tasks crucial for survival. Specialized brain regions allow for quicker response times, minimizing the energy expended across the entire brain. Dedicated areas mean that specific tasks can be processed without the "noise" of other unrelated cognitive activities, leading to improved accuracy and performance in that function. The Fusiform Face Area (FFA) in the human brain is critical for recognizing faces. This specialization is due to the importance of social interactions and recognizing individuals within a community. These regions in the brain are specialized for language production and comprehension, respectively. Their existence highlights the complexity and importance of linguistic abilities in humans. Located in the left fusiform gyrus, the Visual Word Form Area (VWFA) is specialized for recognizing written words, underscoring our species' emphasis on literacy and written communication. The broader range of specialized areas in humans, like those for language or abstract thinking, reflects our diverse skill set and the various cognitive tasks we regularly perform. Chimps, while incredibly intelligent, do not have the same breadth of cognitive specializations. For example, while they can communicate using gestures and sounds, they do not possess the intricate linguistic structures that humans do. Despite functional specialization, the brain remains plastic, meaning it can reorganize and adapt. For instance, if a particular brain region gets damaged, nearby areas might adapt to take over some of its functions. Children's brains are especially plastic. This adaptability allows them to recover more effectively from brain injuries than adults and showcases how functional specialization develops and solidifies over time. Functional specialization is a testament that our brains are both efficient and adaptable. While both humans and chimps have specialized regions catering to their unique needs, the greater diversity of specialized areas in the human brain mirrors our complex societal structures, varied communication methods, and diverse cognitive capabilities.

Evolution, as traditionally understood, is a slow, incremental process where advantageous traits become more common over generations. When considering the brain's functional specialization, one might wonder how complex regions like the Fusiform Face Area (FFA) or the Visual Word Form Area (VWFA) could arise from such a slow and gradual process. However, incremental evolution suggests that these specializations did not appear suddenly but evolved over time as a result of small changes that offered survival and reproductive advantages. For instance, the initial precursors of the FFA would have merely enhanced general visual processing. Over time, as our ancestors became increasingly social, individuals who could quickly recognize and remember faces would have had better social interactions, leading to better survival and reproductive outcomes. Similarly, linguistic abilities, represented by areas like Broca's and Wernicke's, would have evolved from simpler vocalizations to the complex speech we possess today. Each incremental enhancement in these abilities would have conferred evolutionary benefits. The existence of such specialized and intricate brain regions is seen as evidence of purposeful design rather than random evolutionary processes. The sheer complexity and specificity of areas like the FFA or VWFA cannot be solely the result of random mutations and natural selection.  How could such precise functions arise without a guiding hand, especially when considering the intricate interplay between different brain regions?

9. Metabolic Rate

The disparity in energy consumption by the human brain compared to its weight—and in comparison to other primates like chimps—is remarkable.  The heightened energy demands of the human brain suggest significant trade-offs. To sustain such a metabolically expensive organ, early humans would have had to refine their diets and hunting strategies. Incorporating higher-quality, energy-rich foods such as meat or certain types of plant matter would have been a crucial factor in supporting the growth and functioning of our brains. This could also be linked to advancements in tool usage, cooking, and social cooperation in hunting and gathering. The increased energy consumption of the human brain signifies the complex cognitive tasks it undertakes. From abstract thinking, problem-solving, and emotional processing to creative endeavors and intricate communication, the human brain's activities are wide-ranging and intensive. The fact that it demands so much energy underscores the vast array of processes that are constantly occurring, many of which are unique to humans or more developed than in primates. The human brain houses approximately 86 billion neurons, and the connections between them—synapses—are estimated to be over a hundred trillion. This vast network requires energy for maintaining cellular functions, neurotransmission, and synaptic plasticity. Although chimps also have complex brains with billions of neurons, the extent and intricacy of neural connectivity in humans, especially in regions related to higher cognitive functions, may partly account for the elevated energy use. The prolonged developmental period of the human brain, with many aspects of brain maturation continuing well into the twenties, also requires significant energy. This extended period of brain growth, synaptic pruning, and myelination in humans contrasts with the shorter and less energy-intensive developmental periods seen in primates. The human brain is sensitive to temperature changes. A significant amount of energy is allocated to maintain the brain's temperature, ensuring optimal function. Given the size and activity of the human brain, this thermoregulation process can be more energy-intensive than in primates.

The human brain's energy consumption, being roughly 20% of the body's total energy despite comprising only 2% of its weight, is a unique phenomenon, not encountered in the animal kingdom. This disproportionate energy requirement suggests purposeful design, especially considering the delicate balance this creates within the body. The speed with which human ancestors would have had to adapt to meet the brain's metabolic demands challenges the incremental evolution model. The complex interaction between diet, metabolism, and cognition suggests to some a guided process rather than a series of fortuitous evolutionary events. The human brain operates within a narrow range of conditions, with minor deviations in temperature or nutrient supply leading to significant dysfunction. Such a finely-tuned system, especially one with such high metabolic demands, implies intentionality in its design. While many animals have complex brains, none match the human brain's energy demands relative to body size. The absence of any close parallels in the animal kingdom indicates a unique, purposeful design for human cognition.

https://reasonandscience.catsboard.com

20Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Mon Sep 18, 2023 5:08 am

Otangelo


Admin

Objection: Functional magnetic resonance imaging revealed that tool use and syntax in language elicit similar patterns of brain activation within the basal ganglia. This indicates common neural resources for the two abilities between humans, and chimps. 
Reply:  Functional magnetic resonance imaging (fMRI) has opened up new avenues for understanding the neural bases of cognition, and behavior. The finding that tool use and syntax in language elicit similar patterns of brain activation within the basal ganglia in both humans and chimps suggests that there are shared neural resources for these two abilities. This kind of parallelism can be seen as evidence for functional homology, meaning that similar cognitive processes are taking place. However, concluding that these similarities are evidence for common ancestry based solely on fMRI results would be a stretch. When looking at the convergence of tool use and syntax in language that elicits similar patterns of brain activation within the basal ganglia in unrelated species, one has to ponder the likelihood of such an evolutionary setup. One of the most distant and disparate comparisons we can make is between birds and mammals. The avian brain and the mammalian brain are structurally different, yet both exhibit advanced cognitive abilities. For instance, some songbirds have shown remarkable capacities for vocal learning, which bears similarity to the way humans learn to speak. In songbirds like the zebra finch, specific regions known as song nuclei are activated during vocal learning and song production. This functional specialization in the avian brain bears some resemblance to the way certain regions in the human brain, including parts of the basal ganglia, are activated during speech production and syntax processing. However, the architecture of the avian brain is vastly different from that of mammals. Birds lack a neocortex, the six-layered structure responsible for many higher-order cognitive functions in mammals. Instead, they have a nuclear structure, with clusters of neurons organized differently from the mammalian brain. Yet, despite these structural differences, both birds and mammals have sophisticated behaviors that seem to rely on analogous neural processes. This functional convergence, despite significant anatomical divergence, underscores the idea that different pathways can lead to similar cognitive outcomes. However, drawing a direct link between the neural processes of tool use in birds (like the use of sticks by certain crows) and syntax in their vocalizations, and then comparing it to mammals, would be more of a conceptual stretch. The phenomenon of convergence, especially in the realm of evolution, poses perplexing questions that challenge traditional evolutionary explanations. Not only is the appearance of similar traits in unrelated organisms mystifying in itself, but when coupled with genetic distinctions, the puzzle deepens.

Stephen J. Gould, a prominent evolutionary biologist, illustrated the unpredictability of evolutionary trajectories when he remarked, “...No finale can be specified at the start, none would ever occur a second time in the same way, because any pathway proceeds through thousands of improbable stages. Alter any early event, ever so slightly, and without apparent importance at the time, and evolution cascades into a radically different channel.” 1 This statement underscores the inherent randomness and contingency in evolution. Given this unpredictability, the emergence of convergent traits across unrelated organisms seems all the more extraordinary. If, as Gould suggests, a minor deviation in evolutionary history can shift the course of evolution entirely, then how can we account for disparate species arriving at the same complex functionalities or structures?

Moreover, paleontologist J. William Schopf, a leading authority on the origins of life, compounds the enigma with his assertion about the unique nature of intricate biochemical systems. He states, “Because biochemical systems comprise many intricately interlinked pieces, any particular full-blown system can only arise once...Since any complete biochemical system is far too elaborate to have evolved more than once in the history of life, it is safe to assume that microbes of the primal LCA cell line had the same traits that characterize all its present-day descendants.” 2 This perspective highlights a fundamental tension: if complex biochemical systems are so intricate that they can only evolve once, then how do we explain the emergence of functionally analogous systems in genetically distinct organisms? If these systems are truly non-repeatable, then their appearance in diverse lineages becomes an even more formidable challenge to standard evolutionary models. Gould's metaphor of “replaying life’s tape” accentuates the inherent unpredictability of evolution. Yet, the world of biology is rife with examples of convergent evolution where different organisms have independently arrived at similar solutions. This juxtaposition of unpredictability with the repeatability seen in convergent evolution poses a significant dilemma. Schopf's statement emphasizes the notion that once a complex biochemical system arises, its intricate nature precludes it from evolving in the same manner again. This perspective intensifies the mystery surrounding convergent traits found in unrelated organisms. How can similar systems, which are supposed to be unique events in evolutionary history, appear in distinct lineages? Both Gould and Schopf's insights compel us to question the mechanisms traditionally cited in evolutionary theory. Given the phenomenon of convergence, where distinct species independently exhibit similar traits, the explanations of natural selection and random mutations seem insufficient. Just as wheels or engines, fundamental design elements, are utilized across various car models or even different products, the recurrent appearance of analogous features across species might hint at a common design. This design perspective posits that a designer, seeing the efficiency or advantage of a particular feature, has implemented this "solution" in multiple biological "models" throughout nature.

Convergence in diverse species showcases a remarkable pattern that seems to transcend the randomness often associated with evolution. When organisms, despite having distinct evolutionary histories, demonstrate strikingly similar functionalities, it begs the question: How did they arrive at these analogous solutions? Evolution, in its essence, is a process that tends to deteriorate, and in very rare cases, optimize. It gravitates towards solutions that are beneficial and energy-saving, promoting the survival of the organism. So, when different species arrive at similar functions but through distinct pathways, it presents a conundrum. It's like arriving at the same advanced technological solution through completely different routes; this is improbable to the extreme. Behaviors such as the complex tool use seen in certain animals or the vocal learning in songbirds are not just broad strokes of functionality. They are finely tuned, intricate abilities. Achieving such specific outcomes independently in different species suggests a level of precision that's hard to attribute solely to the randomness of genetic mutations.
In biological information, especially the complexities of genetics and neural systems, the parallel emergence of identical functions in different species hints at a guiding principle or a blueprint, that's more consistent than random evolutionary pressures based on natural selection, drift, or gene flow. Evolution, as we understand it, often involves progressive refinements over time. However, the specific and high-level convergences observed in nature seem to leapfrog beyond mere incremental changes. Environmental challenges can push different species towards similar solutions, but the similarity in complex cognitive functions, backed by vastly different brain architectures, is more than just a response to external factors. It appears as if there's a deliberate strategy or underlying design principle at play.

Even if tool use and language syntax activate similar brain regions, the actual neural circuits involved might be different. The broad regions highlighted by fMRI are made up of countless circuits and pathways. Two processes could involve very different circuits even within the same broad region. While fMRI is a powerful tool, it has limitations. It doesn't measure neural activity directly but instead measures changes in blood flow (the BOLD signal). Therefore, it offers a relatively low-resolution picture of brain activity, both in terms of space (where activity is happening) and time (when activity is happening). While tool use and language syntax might activate similar areas, the complexity, nuances, and subtleties of the behaviors are not directly comparable. Human language, for instance, has a depth and complexity that isn't seen in the tool use or communication methods of other species.

1. Gould, S.J. (1989). Wonderful Life: The Burgess Shale and the Nature of History. New York, NY: W.W. Norton & Company. Link. (This pivotal work delves into the mysteries of the Burgess Shale fossils and challenges conventional views on the nature of evolutionary history.)
2. Schopf, J.W. (Ed.). (2002). Life's Origin: The Beginnings of Biological Evolution. University of California Press. Link. (This comprehensive volume, edited by renowned paleontologist J. William Schopf, explores the origins and early evolution of life on Earth.)

https://reasonandscience.catsboard.com

Otangelo


Admin

Differences Between Chimps and Humans - evidence against common ancestry

https://reasonandscience.catsboard.com/t2272-chimps-our-brothers#11280

Comparisons of the levels of morphological and protein divergence between humans and chimps demonstrated that the level of protein divergence was too small to account for the anatomical differences between these two species. To reconcile the level of divergence between proteins and morphology, it has been proposed that morphological divergence is based mostly on changes in the mechanisms controlling gene expression and not changes in the protein-coding genes themselves. The past decades have seen major advances in developmental genetics that have changed the way we approach the origin of morphological characters. These advances have produced several generalizations about the relationship between genetics and phenotypes. Among the most widely recognized is the concept of toolbox genes, that is that different body plans are realized with a conserved set of developmental genes, namely transcription factors and signalling molecules. 20

Humans have 46 chromosomes (23 pairs), while chimps have 48 (24 pairs). The human chromosome 2 appears to have formed as a result of the fusion of two ancestral chromosomes, akin to the chimpanzee's chromosomes 2a and 2b.

Complexity of Fusion 
The fusion of two chromosomes into one (as is hypothesized with human chromosome 2) is a rare event. The specific mechanisms and conditions required to permit such a fusion, and then for the fused chromosome to become fixed in a population, are not entirely understood. This rarity is evidence against a shared ancestry, as it would require this significant event to happen in an isolated population of the shared ancestor, without the trait getting diluted or lost.

Functional Differences
The fusion of two chromosomes leads to significant functional differences between the resulting species. If the two species descended from a common ancestor, such a profound chromosomal difference would make interbreeding and producing fertile offspring challenging or impossible. Chromosomes house vast amounts of genetic information, and the arrangement of this information is crucial for the proper functioning of the organism. The fusion of two chromosomes means a rearrangement of genes, regulatory elements, and non-coding sequences. This rearrangement could lead to variations in gene expression, potential changes in regulatory networks, or even the creation of new genes or regulatory elements at the fusion site. For species with differing chromosome numbers, meiosis—the process that produces eggs and sperm—can become problematic. When these species interbreed, their offspring can end up with an odd number of chromosomes. This can lead to errors in further cell divisions, often resulting in reduced fertility or sterility in the hybrid offspring. For instance, mules, the offspring of horses (64 chromosomes) and donkeys (62 chromosomes), typically have 63 chromosomes and are sterile. If a population with a fused chromosome were to emerge, it might experience reduced interbreeding success with the original population due to chromosomal differences. Over time, these reproductive barriers could accelerate the process of speciation, as the two populations become more genetically isolated from each other. The fused chromosome, if it results in altered gene expression or functionality, might confer specific advantages or disadvantages to individuals bearing it. If the fusion provides a significant benefit in a given environment, it could become prevalent in a population over time. Conversely, if the fusion is disadvantageous, it could get selected against and diminish in the population. The significant genetic differences that arise from chromosomal fusions might mean that the evolutionary pressures and paths for populations with and without the fusion diverge substantially. Over time, the accumulated genetic differences could compound, leading to even more distinct species. The profound chromosomal difference brought about by a fusion event is a significant barrier to continued shared evolution,  supporting the idea of distinct origins of humans and chimps.

Comparative Rarity
Most species retain their chromosomal numbers. When chromosomal changes do occur, they often lead to significant reproductive barriers. The difference between humans having 46 and chimps having 48 chromosomes is evidence of a fundamentally distinct genetic origin, given the rarity of such chromosomal differences in closely related species. The fact that most species maintain consistent chromosomal numbers over time underscores the importance of these structures. Chromosomes house the genetic instructions for every function of an organism. Alterations to their number or structure produce significant ripple effects, influencing everything from individual development to reproductive success. Changes to chromosome number or structure lead to multiple, interconnected consequences throughout an organism's biology. Chromosomal abnormalities affect the proper growth and development of an organism. For instance, humans with Down syndrome have an extra copy of chromosome 21, which results in various developmental and physiological challenges. Differences in chromosome numbers can create barriers to reproduction.  When chromosomal changes arise, they can introduce reproductive complications. In cases where two species with different chromosome numbers mate, their offspring might inherit an atypical chromosome count. These irregularities can hinder the offspring's ability to produce its own viable gametes, essentially creating a barrier to further interbreeding. This reproductive isolation can be a significant factor in the speciation process. The chromosomal difference between humans and chimps is not a minor variation—it's a discrepancy of two whole chromosomes. In the context of closely related species, such a variation suggests a considerable genetic divergence. When we consider how rare it is for closely related species to have such chromosomal disparities, the difference between humans and chimps becomes even more pronounced. If a chromosomal change did arise in an ancestral population, it would likely set that group on a markedly different evolutionary path. The new chromosome number could bring with it unique challenges and opportunities, influencing everything from reproductive strategies to adaptation potentials. Over time, these divergent pressures would lead to the accumulation of other genetic differences, further separating the two groups. Given the rarity and significance of chromosomal number variations among closely related species, the discrepancy between humans and chimps is supportive evidence for fundamentally distinct genetic origins. If the two species did indeed share a recent common ancestor, we might expect more chromosomal uniformity between them, as is observed in many other closely related species.

Genomic Alterations
Both species have had many changes in their genomes, such as rearrangements, additions, or deletions of DNA segments. Think of these as "edits" to their genetic book, where some paragraphs or chapters have been changed, added, or removed. The genomes of species can be thought of as intricate manuscripts. As with any long, complex book, there are bound to be revisions — sometimes sentences are changed, paragraphs added or removed, or whole chapters rewritten. These "edits" come in the form of genetic mutations, rearrangements, additions, or deletions of DNA segments. Both humans and chimps have undergone numerous "edits" in their genetic manuscripts. While some of these changes may be shared, many are unique to each species. Think of these as separate editions or versions of a book. If two books have a multitude of unique edits that are not found in the other, it indicates that they have been written by different authors or have significantly diverged from an original draft. The sheer number and variety of these genomic changes underscore the distinct origins of the two species. Large-scale rearrangements or additions can lead to entirely new functionalities, much like how adding or revising chapters can drastically change a book's narrative or message.

One of the significant differences in the genomes of humans and chimpanzees is in the realm of gene expression and regulatory elements, which control when, where, and how genes are activated.

Concrete Example: HAR1 (Human Accelerated Region 1): The HAR1 region is just 118 base pairs long, but it's notable for having 18 mutations. What's fascinating is that this region is involved in the development of the brain's neocortex, which is responsible for higher-order functions like conscious thought, future planning, and language. In humans, the HAR1 region forms an RNA structure that's vastly different from chimps. This difference in structure suggests a significant divergence in function between the two species, possibly contributing to the vast cognitive differences observed. While both humans and chimps possess a version of HAR1, the considerable alterations in the human version might have played a crucial role in the development of our advanced cognitive abilities.

Pollard, K. S., Salama, S. R., Lambert, N., Lambot, M. A., Coppens, S., Pedersen, J. S., ... & Haussler, D. (2006). An RNA gene expressed during cortical development evolved rapidly in humans. Nature, 443(7108), 167-172. Link. https://www.nature.com/articles/nature05113 (This study explores the rapid evolution of the HAR1 gene in humans, a gene expressed during cortical development.)

In this paper, Pollard and colleagues describe how the HAR1 region differs significantly between humans and chimpanzees. This is a concrete example of how even small genomic "edits" can lead to potentially profound differences in the biology and capabilities of two species. The changes in genes related to brain development, immunity, or metabolism result in radically different physiologies and capabilities.  When observing the diverse modifications in the genomes of both humans and chimps, one can draw an analogy to two intricate pieces of machinery or sophisticated software applications. Each machine or software application is designed for a specific purpose. They might share some basic components or foundational code, but the specificities of their design show a targeted purpose. When a designer embarks on creating multiple products, he often uses a foundational template or set of core components to ensure efficiency and functionality. But it's the subtle variations, the nuanced differences, that reveal the true genius and intention behind each creation. These variations aren't random or accidental; they're deliberate, crafted with foresight for specific purposes. Consider the world of automobiles. Many cars share similar foundational components: engines, wheels, transmissions, and so forth. Yet, a sports car is distinct from an SUV not just in appearance but in function. The designer of the sports car envisions speed, aerodynamics, and performance, optimizing every part with that intent in mind. Conversely, the SUV is designed with space, ruggedness, and versatility at the forefront. Both vehicles stem from the basic concept of transportation, but their design specifics clearly reflect different purposes. Similarly, in the realm of software, a programmer might utilize the same base code to develop different applications. Yet, one application could be a sophisticated graphic design tool, while another could be a database management system. Both applications might contain similar foundational algorithms or libraries, but they have been intentionally modified and expanded upon to serve distinct functions. This analogy can be drawn closer to the genetic similarities and divergences seen between humans and chimps. Yes, they might share a foundational "code," but the precise "tweaks" and "modifications" in their DNA suggest distinct intentions for each. These aren't mere byproducts of chance but rather indications of a purposeful design. It's as though a mastermind, equipped with immense knowledge and foresight, has used a foundational template but introduced critical variations to ensure that each species is perfectly designed for the designer's goals and purpose.

Imagine two master engineers who, using their vast knowledge, craft two machines. Both machines have gears, circuits, and power sources, but one is tailored for deep-sea exploration, while the other is built for navigating the vastness of outer space. The sea-exploring machine is fitted with tools and sensors that allow it to withstand high pressure and detect changes in water composition. The space machine, on the other hand, is designed to operate in a vacuum, with radiation shields and equipment to analyze alien atmospheres. While they share fundamental design elements due to the engineers' shared knowledge, their specific and intricate modifications point towards an intentional design for distinct environments. In a similar vein, both humans and chimps might have genetic "tools" and "features" that suggest a certain foundational design principle. Still, the multitude of unique "edits" in their genomes are intentional modifications. It's as though the story of each species has been meticulously crafted, chapter by chapter, to ensure they thrive in their respective narratives, rather than being mere products of random or passive changes. If two books were being concurrently edited by the same author, you'd expect recent changes to be consistent between them. However, many of the recent "edits" in the human and chimp genomes are not shared, suggesting separate or independent origins.

Mobile Elements
Both species have "mobile elements" in their DNA, which can move around and create changes. Humans and chimps have different numbers and types of these stickers. Mobile elements, or transposons, are sequences in DNA that can change their position within the genome. Picture these as stickers in a scrapbook that, rather than being permanently affixed to a page, can move around and even duplicate themselves in the process. This movement can influence the function of genes, potentially leading to changes. When we compare the genomes of humans and chimps, one fascinating discovery is the shared insertion sites of some of these transposons. In other words, in both species, certain "stickers" are found in the same positions in their respective "scrapbooks." From an evolutionary standpoint, the shared sites are often cited as evidence for a common ancestry. The reasoning is that the odds of the same mobile element inserting itself independently at the exact same position in two separate species are extremely low. However, the shared insertion sites are indicative of a shared template or design plan. If we consider an architect who designs multiple buildings, it's plausible that certain features or designs are intentionally repeated across different structures because they serve a particular purpose or function. Similarly, the shared transposon sites reflect an intentional design element optimized for a specific function in both humans and chimps.

The shared transposon insertion sites between humans and chimps are primarily associated with classes of mobile elements like Alu sequences, LINEs, and SVA elements. These elements have been found at the same positions in the genomes of both species, Alu Sequences are short stretches of DNA (about 300 nucleotides long) that have proliferated to the extent that they make up about 10% of the human genome. In both humans and chimps, there are over a million copies of Alu sequences. A significant number of these are located at the same genomic positions in both species. While new Alu insertions can happen, the shared positions between humans and chimps can be intentionally placed markers.

The shared insertion sites have been mentioned and popularized as presenting a compelling case for shared ancestry from an evolutionary perspective. But there are alternative possible, plausible explanations.  If the locations of these Alu insertions are crucial for some cellular or molecular function, then their shared presence in both human and chimp genomes is a feature of intentional design. Specific genomic loci might be "hotspots" for insertions because they offer functional advantages, such as influencing gene regulation or expression. If these sites provide a benefit, it makes sense that both humans and chimps have them, irrespective of common ancestry.  Such insertions, found at the same relative location in both genomes, are powerful evidence for functionality when they have discernible roles in gene regulation or other genomic functions. 

Several known functions of Alu elements include:

Influence on Gene Regulation: Alu elements can act as transcriptional enhancers or silencers, influencing the expression levels of nearby genes.
Alternative Splicing: Alu sequences in exons and introns influence alternative splicing patterns, resulting in diverse transcript variants. This can lead to the generation of various protein isoforms from a single gene.
Genomic Structural Variation: Alu elements can promote non-allelic homologous recombination events, which may result in genomic structural variations like deletions, duplications, and inversions.
Influence on Protein Coding: On rare occasions, parts of Alu sequences can be incorporated into mature mRNA and get translated, impacting protein function or creating novel peptides.
miRNA Target Sites: Alu elements can provide binding sites for microRNAs (miRNAs), small non-coding RNAs that regulate gene expression post-transcriptionally.
DNA Methylation: Alu elements can be sites for DNA methylation, an epigenetic modification that can influence gene expression. Alu-associated methylation can have implications in various biological processes, including aging and cancer.
Promotion of DNA Double-Strand Break Repair: There's evidence suggesting that Alu elements can participate in the DNA damage response, particularly in non-homologous end joining, a pathway for repairing DNA double-strand breaks.
Genome Evolution: Due to their repetitive nature and capacity for mobilization, Alu elements play a role in genome evolution by promoting genomic diversity.
Formation of Nuclear Domains: Alu elements have been implicated in the organization of certain nuclear domains which influence gene expression and other nuclear processes.
Stress Response: Some Alu elements are transcribed in response to various stresses, and their RNA products might play roles in cellular stress responses.
Source of Genetic Diseases: Mis-insertion or unequal recombination involving Alu elements can lead to genetic diseases.

Here's a notable paper on this topic:

Polak, P., & Domany, E. (2006). Alu elements contain many binding sites for transcription factors and may play a role in regulation of developmental processes. BMC Genomics, 7(1), 133. Link. https://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-7-133 (This study explores the high frequency of transcription factor binding sites within Alu elements. Given that many of these Alu insertions are shared between humans and chimps, this study postulates that they may have roles in the regulation of developmental processes in both species.)

This paper not only sheds light on shared Alu insertions but also delves into their potential functional roles. The presence of shared insertion sites with functions like transcription factor binding suggests that these are not mere byproducts of random insertion events, but rather potentially conserved elements that play a role in the shared biology of humans and chimps.

There is also the observed influence of Alu sequences on gene regulation, expression, splicing, and other genomic functions.  Influence on Gene Regulation and Expression:

Batzer, M. A., & Deininger, P. L. (2002). Alu repeats and human genomic diversity. Nature Reviews Genetics, 3(5), 370-379. Link. https://www.nature.com/articles/nrg798 (This comprehensive review highlights the impact of Alu sequences on genomic diversity and underscores their potential to influence gene expression and regulation.)

Sorek, R., Ast, G., & Graur, D. (2002). Alu-containing exons are alternatively spliced. Genome research, 12(7), 1060-1067. Link. https://genome.cshlp.org/content/12/7/1060.full (This study demonstrates that Alu sequences within exons can influence alternative splicing patterns, leading to diverse transcript variants.)

Bejerano, G., Lowe, C. B., Ahituv, N., King, B., Siepel, A., Salama, S. R., ... & Haussler, D. (2006). A distal enhancer and an ultraconserved exon are derived from a novel retroposon. Nature, 441(7089), 87-90. Link. https://www.nature.com/articles/nature04696 (The paper identifies retroposon-derived sequences, including those similar to Alu elements, which have taken on critical regulatory roles in the human genome, particularly in neural gene expression.)

Each of these studies sheds light on the functional significance of Alu sequences, providing a plausible reason for their presence and conservation in specific genomic locations. These shared features are evidence for purposefully placed elements that contribute to the functionality and robustness of the genome.

Alu insertions
There are thousands of shared Alu insertions between humans and chimpanzees. Estimates suggest that humans and chimps share approximately 7,000 to 8,000 Alu element insertions. These shared insertions are often used as evidence in support of a common ancestor for the two species. Both evolution and design can operate under constraints. In the case of Alu insertions, there might be only a limited number of sites that are permissible or optimal for insertion. From a design perspective, these constraints could be imposed to ensure genomic stability, proper function, or other essential attributes. Hence, the presence of Alu sequences in the same loci across species are warranted to be seen as a feature of design operating within specific constraints, rather than evidence of common ancestry. If certain insertion sites offer advantages, it's possible that these sites could be chosen for both species due to their benefits, even without shared ancestry. The sheer complexity and intricate order of the genome might necessitate specific features to be in certain places. If one views the genome as a meticulously crafted system, then every part, including Alu insertions, has its designated place for the system to function optimally. The presence of these insertions in the same places in both species might be evidence of an underlying blueprint or pattern, much like how different models of a device might have components in the same locations because they are all based on a foundational design.

LINEs (Long Interspersed Nuclear Elements) 
LINEs are longer sequences, typically around 6,000 nucleotides. LINE-1 (L1) is the most common type in mammalian genomes. There are shared L1 insertion sites between humans and chimps, again suggesting either a common ancestral origin or an intentional design.  The idea of "hotspots" or preferred regions for transposable element insertions isn't new. These hotspots can be areas that are more accessible to the transposable element machinery, or they might be regions where insertion doesn’t result in a lethal effect, and thus these insertions can be passed on to the next generation.

Speek, M. (2001). Antisense promoter of human L1 retrotransposon drives transcription of adjacent cellular genes. Molecular and cellular biology, 21(6), 1973-1985.  https://mcb.asm.org/content/21/6/1973
This study explores the regions where L1 elements integrate and suggests that certain genomic regions might be more conducive to these insertions due to their regulatory potential.

Boissinot, S., & Furano, A. V. (2001). Adaptive evolution in LINE-1 retrotransposons. Molecular biology and evolution, 18(12), 2186-2194. https://academic.oup.com/mbe/article/18/12/2186/1050194
This paper discusses insights into the regions of the genome that might act as "hotspots" for LINE-1 insertions. 

If L1 insertions were purely a result of common ancestry, the expectation would be that other closely related species would also share these same insertions. However, looking into the broader spectrum of primates and mammalian evolution, L1 activity and its patterns are not uniformly conserved across all lineages. Some key findings in various scientific studies have highlighted these discrepancies:

Salem, A. H. ... & Batzer, M. A. (2003). Alu elements and hominid phylogenetics. Proceedings of the National Academy of Sciences, 100(22), 12787-12791.
Link. https://www.pnas.org/doi/10.1073/pnas.2133766100 (This paper explored Alu elements and their relevance in understanding hominid relationships. The study highlighted that the distribution of Alu elements is not always consistent with the accepted phylogenetic tree.)

Boissinot, S., Chevret, P., & Furano, A. V. (2000). L1 (LINE-1) retrotransposon evolution and amplification in recent human history. Molecular biology and evolution, 17(6), 915-928.
https://pubmed.ncbi.nlm.nih.gov/10833198/ (This study on L1 elements showcases that the recent evolutionary amplification patterns of L1 are not consistent across all human populations.)

Khan, H., Smit, A., & Boissinot, S. (2006). Molecular evolution and tempo of amplification of human LINE-1 retrotransposons since the origin of primates. Genome research, 16(1), 78-87.
Link. https://genome.cshlp.org/content/16/1/78.full (This paper examined the evolutionary history of LINE-1 elements in humans and found that their amplification has not been steady over time and varies considerably among primates.)

Locke, D. P.... & Gibbs, R. A. (2011). Comparative and demographic analysis of orangutan genomes. Nature, 469(7331), 529-533.
Link. https://www.nature.com/articles/nature09687 (In this study, orangutan genomes were analyzed, revealing significant differences in the distribution and activity of mobile elements, including LINE-1, when compared to humans and other primates.)

These studies reveal that while there might be shared L1 insertions between humans and chimps, the broader context of primate evolution presents discrepancies. These discrepancies in shared L1 sites among a wider spectrum of primates indicate that there's more to the story than just a straightforward narrative of common ancestry based solely on L1 insertion similarity.  If shared L1 insertion sites between humans and chimps have been demonstrated to serve essential regulatory or structural functions in the genome, it hints at an intentional design. Evolution by natural selection operates on functionality; it doesn't have foresight. In contrast, intentional design can place elements in anticipation of future needs or to serve intricate, multifaceted roles. The selection of studies presented covers a wide spectrum of the roles and implications of LINE-1 (L1) elements in the genome. At a holistic level, they make a compelling case that these elements are not mere genomic "junk" or arbitrary remnants of ancient viral insertions, but rather possess significant functionalities that might be better explained by a design perspective.

Speek (2001): The ability of the antisense promoter in the L1 retrotransposon to drive transcription of adjacent genes underscores the importance of L1 in influencing gene expression patterns. Such a feature can be likened to a regulatory mechanism, one that has been deliberately positioned to optimize the expression of essential genes. 1
Khan et al. (2006): If L1 elements were simply remnants of our evolutionary history, one would expect them to be uniformly amplified across primates. However, the study suggests that their amplification has been selective, hinting at some functional significance which has undergone specific pressures to maintain or change their presence. 2
Faulkner & Carninci (2009): Contrary to the notion that mobile elements like L1 are "selfish" and exist primarily for their propagation, this research elucidates their "altruistic" roles that benefit the host. Such complex dual roles—both selfish and altruistic—are indicative of a design with multifaceted purposes.3
de Koning et al. (2011): The staggering presence of repetitive elements in the human genome, including L1, challenges the idea that these sequences are merely evolutionary leftovers. Their abundance suggests an orchestrated design, with each element playing a part in the genomic symphony. 4
Fort et al. (2014): The involvement of retrotransposons, including L1, in maintaining pluripotency of mammalian stem cells, is a testament to their essential function. It's challenging to dismiss such a pivotal role as a mere coincidence arising from shared ancestry.5
Lewinski & Bushman (2005): By diving into the mechanics and implications of retroviral DNA integrations akin to L1, this review encapsulates the myriad ways through which these elements impact genomic structure and function. The precision and intricacy of these mechanisms point towards a well-calibrated system, which could be seen as a hallmark of design.6

The genome operates as a complex system with multiple layers of regulation and interaction. Shared L1 insertions that are found in functionally crucial regions of the genome (e.g., gene regulatory networks) in both species can be seen as evidence of a shared design template. Just as an engineer might use a specific component in multiple devices because of its reliability and function, the shared L1 sites can be viewed as essential components in the genomic machinery. If the shared L1 insertions work in coherence with other genomic elements (like Alu sequences or specific genes) in a way that creates a harmonized system in both humans and chimps, it would suggest a design principle that values integration and harmony in genomic operations.

SVA Elements
These are newer, composite elements made up of sequences from other transposons. They're called SVAs because they contain segments from SINEs, VNTRs, and Alu sequences. While there are fewer SVAs than Alus or LINEs, shared insertion sites can still be found between humans and chimps.

Additionally, it's essential to note that while many insertion sites are shared, there are also numerous sites unique to each species, highlighting the distinctiveness of their genetic makeup. These unique sites, along with the shared ones, contribute to the overall complexity and specificity of each species' genome.

Gene Differences
The genes, or instruction sets, for things like smell (olfactory receptors) differ between the two species. Both have unique mutations in genes that deal with immune responses and how cells recognize each other. Humans have specific mutations related to speech and brain size, while chimps have their own unique mutations. Apart from genes that instruct how to build and operate a body, there are other DNA segments, "non-coding sequences", that help control how these genes work. Humans have special regions called HARs and HACNs. These areas are especially important for brain development and function. Both species have various pericentric inversions, as well as a multitude of deletions, insertions, and copy number variations. The complexity and multitude of these alterations suggest separate genetic pathways and histories, rather than modifications from a shared ancestor. There are species-specific mutations and differing repertoires of genes related to olfaction, immunity, sialic acids metabolism, and brain development. The unique genes and mutations in each species might suggest they were crafted for specific purposes, hinting at separate origins. Differences exist in the coding sequences of both species, such as the divergent genes related to immunity and cell recognition. The unique sets of protein-coding genes in each species may imply separate genetic blueprints, supporting the idea of separate origins.

Neurological Distinctions
Humans have unique white matter tracts, with changes in their architecture, implying different neural connections. This impacts cognitive functions and our ability for abstract thinking, planning, and complex language.
Distinct genes related to neurotransmitters affect behavior, cognition, and social interactions differently in the two species.

White Matter Tracts and Cognitive Function
Human brains show a distinctive pattern of myelination, particularly in the white matter tracts. Myelin is crucial for rapid signal transmission in neural pathways. Enhanced myelination in humans, especially in the frontal lobes, contributes to quicker cognitive processing and advanced decision-making capabilities. Arcuate Fasciculus is a white matter tract connecting the Broca's area and the Wernicke's area in the human brain, essential for language comprehension and production. While chimps do have an arcuate fasciculus, it's less developed and doesn't have the same connectivity, which may partly explain why they don't possess complex language capabilities like humans.

The Significance of the Arcuate Fasciculus AF in Humans
The AF is not just a simple connector between Broca's and Wernicke's areas, but serves as an essential highway for a plethora of linguistic processes. This includes semantics (meaning), syntax (sentence structure), prosody (intonation and rhythm), and phonological processing. The development and sophistication of the AF in humans facilitates the nuanced and multifaceted nature of our language. Research using diffusion tensor imaging has revealed that the human AF consists of both anterior-to-posterior and posterior-to-anterior segments, indicating a bidirectional flow of information. This two-way communication is essential for the real-time feedback and rapid processing required for fluent speech and comprehension. Beyond just Broca's and Wernicke's areas, the AF interacts with other parts of the brain, such as the inferior parietal lobule, involved in tasks like reading and number processing. This suggests its role in integrating diverse cognitive functions, not just speech. The level of sophistication and intricacy in the human AF, compared to its simpler counterpart in chimps, doesn't lend itself easily to gradual evolutionary narratives. It's hard to envision intermediary stages where a partially formed AF would offer significant evolutionary advantages. For the AF to evolve to support language, language itself would need to co-evolve with the tract. This simultaneous evolution of brain structures and sophisticated linguistic capabilities presents a chicken-and-egg problem. Which came first: the linguistic need or the neural structure? If the AF in earlier hominins or common ancestors of humans and chimps was underdeveloped (similar to chimps), they would likely have alternative neural pathways for communication. Evolutionary development of the AF would render these pathways redundant, which is inefficient from an evolutionary perspective. The AF's intricate architecture in humans, with its bidirectional pathways and connections to multiple brain regions, suggests a purposeful design tailored for complex linguistic and cognitive tasks. This is less about a mere enlargement or modification of an existing structure and more about a reimagining of its role and capabilities. The disparity in the development and functionality of the AF between humans and chimps indicates distinct blueprints or origins, rather than one species being a modified version of the other. The brain operates as a holistic network. A change in one area (like the AF) can impact various other regions and functions. The seamless integration of the AF in the human neural framework underscores the idea of a coordinated and thoughtfully crafted design, as opposed to haphazard evolutionary additions.

Corpus Callosum Connectivity
The corpus callosum in humans supports enhanced interhemispheric communication, critical for complex tasks like reading and abstract thinking. Chimps, while having a corpus callosum, exhibit differences in their architecture and function. The corpus callosum is the largest white matter tract in the human brain and plays a pivotal role in integrating functions of the left and right cerebral hemispheres. Its intricate design in humans compared to other primates like chimps raises profound questions about the nature and origin of its development.  The corpus callosum facilitates rapid and complex communication between the two hemispheres. This integration enables humans to perform tasks that require the simultaneous engagement of both hemispheres, such as understanding metaphors, where the left hemisphere processes the language and the right processes the abstract concept. Motor and Sensory Integration plays a role in coordinating motor outputs and sensory inputs between the hemispheres. This is evident in tasks requiring hand-eye coordination, where both hemispheres must work in tandem. The right hemisphere plays a significant role in processing emotions. Through the corpus callosum, emotional signals can be rapidly transferred and processed in the context of language and logic located predominantly in the left hemisphere.

While chimps have a corpus callosum, there are distinctions: The human corpus callosum, when adjusted for brain size, is thicker and contains more axons. This means more information can be transferred and at a quicker rate in humans. The patterns of connectivity, and thus the specific functions facilitated by the corpus callosum in chimps, may be different from those in humans, reflecting the disparate cognitive capabilities between the species.
Given the profound impact of the corpus callosum on human cognition and its intricate design, it's challenging to envision intermediary stages of its evolutionary development where incremental advantages would be provided.
The brain isn't just about having connections, but about having the right ones. For every neuron in the brain, there are approximately 10,000 synaptic connections to other neurons. The mathematical permutations for these connections are staggering. Even a slight miswiring could lead to non-functionality or malfunctions. A fully functional corpus callosum emerging through random mutations seems immensely improbable. The evolution of the corpus callosum's advanced design would necessitate the simultaneous evolution of other brain regions and functionalities that it interfaces with. Such a synchronized evolution poses a significant challenge to explain. The precise and meticulous design of the human corpus callosum points to intentional crafting. Its integration with other brain areas seems purposefully coordinated for complex cognitive functions. The capabilities facilitated by our corpus callosum, like abstract thinking, are uniquely human. Such distinctive features hint at a separate origin or blueprint rather than an incremental development from a primate ancestor.

Neurotransmitters and Behavior
The DRD4 gene, which codes for the dopamine receptor, has variations in humans linked with novelty-seeking behavior. Chimps have different versions of this gene, leading to differences in risk-taking and exploratory behavior.
Variations in genes regulating serotonin can influence social behavior. Humans have specific genes that underpin our cooperative nature and societal structures, while chimps possess versions that support their more hierarchical and territorial social systems. HARs (Human Accelerated Regions) are segments of the genome that are often involved in gene regulation, especially during brain development. microRNAs are small RNA molecules that play a crucial role in gene regulation. Humans and chimps have differences in the expression and function of several microRNAs, especially those implicated in brain function and development. Methylation patterns, an epigenetic mechanism, can vary between humans and chimps. Differences in these patterns can influence how genes are turned on or off, leading to divergence in traits and functionalities. Gene regulatory networks often involve feedback loops, where the product of a gene can influence its own expression or that of other genes. Differences in these loops between the species can lead to a cascade of changes, drastically altering biological outcomes. Given the complexity of these networks, even minor initial differences imply in significant divergence. While humans and chimps share a substantial portion of their DNA, the intricate differences in neural architecture, neurotransmitter regulation, and gene regulatory networks strongly suggest separate evolutionary trajectories. These distinct pathways and the resulting differences in cognition, behavior, and social structures provide powerful evidence against a singular shared ancestry.

Further differences
Humans and chimps have different dietary requirements and digestion mechanisms. Chimps have a more robust gut to process a varied diet, including raw plant materials, whereas humans are adapted to eat cooked food. Chimps have unique genes catering to their knuckle-walking motion, while humans possess genetic codes for upright bipedalism, affecting everything from our pelvis structure to foot arches. Humans have an extended childhood and adolescence phase compared to chimps. Genetic differences dictate the human brain's slower maturation and our longer reproductive cycle. The genetic, epigenetic, manufacturing, and regulatory information and signaling pathways and information result in different lengths of pregnancies between the two species, with humans having a notably longer gestation period. While both rely heavily on vision, humans have specific genes related to trichromatic vision, aiding in discerning a broader spectrum of colors. Chimps, although having good vision, don't have the same color discernment abilities. Genetic differences result in variations in taste bud receptors. For instance, humans are sensitive to a broader range of tastes, making us more discerning eaters. Interestingly, chimps have a faster wound-healing process than humans. Distinct genetic pathways provide them with a more efficient recovery mechanism.
While humans might be susceptible to certain diseases, chimps might be naturally immune to them, and vice-versa. This can be attributed to species-specific immune-related genes. Differences in DNA methylation, a mechanism used to control gene expression, between humans and chimps points to different evolutionary trajectories. Studies suggest that certain genes mutate at different rates in humans and chimps, indicating separate evolutionary trajectories.

Further reading: The origin of speech, by evolution, or design? 
https://reasonandscience.catsboard.com/t1334-language-the-origin-of-language#8230

1. Speek, M. (2001). Antisense promoter of human L1 retrotransposon drives transcription of adjacent cellular genes. Molecular and Cellular Biology, 21(6), 1973-1985. Link.
This paper demonstrates that the antisense promoter in the L1 retrotransposon can drive the transcription of adjacent cellular genes. This shows that L1 can influence gene expression patterns.
2. Khan, H., Smit, A., & Boissinot, S. (2006). Molecular evolution and tempo of amplification of human LINE-1 retrotransposons since the origin of primates. Genome research, 16(1), 78-87. Link.
This study reveals that LINE-1 elements, such as L1, have not been uniformly amplified across primate evolution. Their distribution and activity patterns suggest selective pressures, indicating their potential functional significance.
3. Faulkner, G. J., & Carninci, P. (2009). Altruistic functions for selfish DNA. Cell cycle, 8(18), 2895-2900. Link.
This study showcases the broader perspective that mobile elements, including L1, have roles beyond "selfish" propagation. They often have "altruistic" roles beneficial for the host organism, like gene regulation.
4. de Koning, A. P., Gu, W., Castoe, T. A., Batzer, M. A., & Pollock, D. D. (2011). Repetitive elements may comprise over two-thirds of the human genome. PLoS genetics, 7(12), e1002384. Link.
This comprehensive study suggests that a significant portion of the human genome is comprised of repetitive elements, including L1. The sheer abundance of these elements points towards their potential functionality.
5. Fort, A., Hashimoto, K., Yamada, D., Salimullah, M., Keya, C. A., Saxena, A., ... & Carninci, P. (2014). Deep transcriptome profiling of mammalian stem cells supports a regulatory role for retrotransposons in pluripotency maintenance. Nature genetics, 46(6), 558-566. Link.
This study provides a deep insight into the transcriptional profile of mammalian stem cells. It supports the idea that retrotransposons, including L1, play a role in maintaining pluripotency.
6. Lewinski, M. K., & Bushman, F. D. (2005). Retroviral DNA integration—mechanism and consequences. Advances in genetics, 55, 147-181. Link.
This review covers the mechanics and consequences of retroviral DNA integration, including elements similar to L1. It underscores the potential functional implications of such insertions.

https://reasonandscience.catsboard.com

22Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Fri Mar 22, 2024 1:40 pm

Otangelo


Admin

Modern Science refutes the Evolutionary theory

2023/08/09

Huge differences between human/chimp lncRNAs refute the theory of Evolution

LncRNAs determine the fate of stem cells, tissue type's identity, organ function, and even body plan

https://www.frontiersin.org/articles/10.3389/fgene.2020.00277/full

Excerpt: "Pluripotent stem cells have broad applications in regenerative medicine and offer ideal models for understanding the biological process of embryonic development and specific diseases. Studies suggest that the self-renewal and multi-lineage differentiation of stem cells are regulated by a complex network consisting of transcription factors, chromatin regulators, signaling factors, and non-coding RNAs. It is of great interest to identify RNA regulatory factors that determine the fate of stem cells. Long non-coding RNA (lncRNA), a class of non-coding RNAs with more than 200 bp in length, has been shown to act as essential epigenetic regulators of stem cell pluripotency and specific lineage commitment. In this review, we focus on recent research progress related to the function and epigenetic mechanisms of lncRNA in determining the fate of stem cells, particularly pluripotency maintenance and lineage-specific differentiation."

My comment: LncRNAs regulate e.g. cellular differentiation processes.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8143134/Excerpt: "Long non-coding RNAs (lncRNAs) are a large class of gene transcripts that do not code proteins; however, their functions are largely unknown and many new lncRNAs are yet to be discovered. Taking advantage of our previously developed, super-fast, novel lncRNA discovery pipeline, UClncR, and rich resources of GTEx RNA-seq data, we performed systematic novel lincRNA discovery for over 8000 samples across 30 tissue types. We conducted novel detection for each major tissue type first and then consolidated the novel discoveries from all tissue types. These novel lincRNAs were profiled and analyzed along with known genes to identify tissue-specific genes in 30 major human tissue types. Thirteen sub-brain regions were also analyzed in a similar manner. Our analysis revealed thousands to tens of thousands of novel lincRNAs for each tissue type. These lincRNAs could define each tissue type’s identity and demonstrated their reliability and tissue-specific expression."

My comment: LncRNAs define also different tissue type's identities.

https://www.sciencedirect.com/science/article/pii/S2589555920301117Excerpt: "Long non-coding RNAs (lncRNAs) are important biological mediators that regulate numerous cellular processes. New experimental evidence suggests that lncRNAs play essential roles in liver development, and normal liver physiology" My comment: LncRNAs also regulate organ development and function. https://academic.oup.com/mbe/article/32/9/2367/1030095Excerpt: "A high diversity of transiently expressed lncRNAs also was present during the first 24 h of metamorphosis, when the larval body plan is being resculpted into the juvenile/adult body plan. Finally, the number of expressed lncRNAs increased at the establishment of the juvenile body plan and in the adult."My comment: LncRNAs are involved even in the regulation of body plans.The number of DIFFERENT lncRNAs in a human body according to NONCODEv5 is 172,216. However, the number of different lncRNAs in a chimp body is only 18,604. LncRNAs play a very significant role in cellular differentiation, tissue type regulation, organ function, and even body plan. We should also remember that the number of different lncRNAs in a human body is almost 9 times higher than the number of protein-coding genes. Studies have also revealed that human/chimp lncRNAs are very different (non-conserved). Evolution believers claim that lncRNAs have evolved through mutations (HAR = human accelerated regions). However, medical science is aware that lncRNAs don't tolerate mutations:https://www.qmul.ac.uk/blizard/about/news/items/long-noncoding-rnas-in-neurological-diseases.htmlExcerpt: "Because of their important role in gene expression regulation, it should not be surprising to assume that any malfunction of lncRNAs, for example due to mutations, could have even serious consequences on the normal development of body organs. In fact, this is exactly what has been found by comparing the sequences of these RNAs in normal people versus diseased individuals.In the field of neurology, mutations in lncRNAs have been associated with abnormalities of neurological development or neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s and ASD (Autism spectrum disorder). Given the high personal and social impact of these diseases, it is very important to understand how these RNAs carry out their activity and what goes wrong following disease-causing mutations." Summary and conclusions:

LncRNAs have a crucial epigenetic role in several cellular processes such as stem cell differentiation, tissue type regulation, organ function, and body plan. DNA doesn't determine stem cell fate, tissue type, organ function, or body plan. DNA is passive information used in a sophisticated way for the cell to construct active RNA molecules. The number of different lncRNAs in a human body is almost 9-fold compared to that of chimps. It's ridiculous to claim that this huge difference in the number of human lncRNAs could have arisen after a chromosome fusion because biological information is always reduced during chromosome fusions. LncRNAs don't tolerate mutations. It's impossible for lncRNAs to evolve through mutations. Science is not aware of positive mutations in these regulatory lncRNAs. We are not related to chimps.

https://sciencerefutesevolution.blogspot.com/2023/08/huge-differences-between-humanchimp.html?fbclid=IwAR2Kb4W9pKz6Xh_4A8BcuB4DMRtBI1JUYQ0UmvpdEocQNQXD2mzDcUoUEZQ

https://reasonandscience.catsboard.com

23Chimps, our brothers ?  Empty Re: Chimps, our brothers ? Sat Apr 06, 2024 11:08 am

Otangelo


Admin

Challenging Evolutionary Narratives: Genetic Disparities and Brain Complexity between Humans and Apes

The Disputed Similarity Between Human and Chimpanzee DNA

The oft-cited statistic that human and chimpanzee DNA are 99% similar has been subject to significant scrutiny and debate within the scientific community. This widely-reported figure, originating from a study in the early 1970s, has been increasingly challenged as more advanced genetic analysis techniques have been developed.

According to Dr. Todd Preuss, an Associate Research Professor at Emory University's Yerkes National Primate Research Center,

It is now clear that the genetic differences between humans and chimpanzees are far more extensive than previously thought; their genomes are not 98% or 99% identical.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386880/

This revision in the estimated DNA similarity between humans and chimpanzees has significant implications for the evolutionary relationships between the two species. The closer the genetic similarity, the more plausible the macroevolutionary transition from a chimpanzee-like ancestor to modern humans. However, the increasing divergence in the genetic makeup of humans and chimpanzees casts doubt on the commonly held evolutionary narrative.
The biblical perspective, which portrays humans and apes as distinct created kinds, appears to find support in the emerging genetic evidence that challenges the previously assumed high degree of similarity. This shift in scientific understanding undermines the evolutionary argument that relies on a close genetic relationship between humans and chimpanzees as a foundation for macroevolution. It is important to note that the scientific debate around the precise percentage of similarity between human and chimpanzee DNA is ongoing, and the specific numbers reported may continue to evolve as new research and analytical techniques emerge. However, the growing consensus that the similarity is significantly lower than the oft-cited 99% figure lends credence to the biblical account of distinct human origins. This evolving scientific landscape highlights the need for a nuanced and critical examination of the relationship between biblical and scientific claims, rather than relying on outdated or potentially flawed data. The discussion surrounding human-chimpanzee DNA similarity exemplifies the dynamic nature of scientific understanding and the importance of keeping pace with the latest findings when evaluating competing perspectives on the origins of humanity.

The Flaws in the Evolutionary Narrative of the Human Brain

The prevailing evolutionary account of the human brain's origins has long been touted as a scientific triumph, confirming the predictions of Darwin and Huxley regarding our close relationship to the great apes. However, a closer examination of the evidence reveals significant problems with this evolutionary narrative.

Improbable Neuronal Development: The claimed step-wise expansion of the hominid brain, from approximately 450 ml to the modern 1,350 ml average, is purported to have occurred through gradual, evolutionary processes. Yet, the sheer number of new neurons and synaptic connections required - up to 166,000 per generation - strains the credibility of undirected, random mutation and natural selection as the driving forces. The probability of randomly generating the precise specifications needed for a functioning brain appears vanishingly small.

Neuronal Increase per Generation:
- The hominid brain is estimated to have increased from 450 ml to the modern 1,350 ml average.
- Assuming a 10-year average breeding age, there would have been approximately 350,000 generations over the 3.5 million year period.
- The increase in neurons during this time is estimated to be around 58 billion.
- Dividing the 58 billion neuron increase by the 350,000 generations yields an average of 166,000 new neurons per generation.

Neuronal Interconnectivity:
- Each neuron in the human brain can have up to 100,000 synaptic connections.
- To maintain proper brain function, these new neurons would need to form the correct 166,000 x 100,000 = 16.6 billion new synaptic connections per generation.

Neuronal Diversity:
- The human brain contains approximately 3,000 different types of neurons, each with its own specialized features and functions.
- For the brain to develop properly, each new neuron added would need to be of the correct type, positioned appropriately, and integrated into the existing neural network.

Probabilistic Challenges:
- Generating the precise specifications for 166,000 new neurons, each with 16.6 billion correct synaptic connections, and ensuring they are of the appropriate 3,000 neuronal types, appears astronomically improbable through random mutation and natural selection alone.
- The likelihood of randomly producing such a complex, integrated system is vanishingly small, casting serious doubt on the evolutionary account.

Language and Communication: Humans have a highly developed and complex system of language that allows for abstract thought, symbolic communication, and the transmission of culture across generations. While other apes can communicate using gestures, vocalizations, and even some rudimentary forms of sign language, human language is unparalleled in its complexity and versatility.

Irreducible Complexity: The human language faculty is an excellent example of irreducible complexity, where the various components cannot be easily separated or evolved independently.
Phonology and Speech Production: The ability to produce speech sounds requires the precise coordination of multiple brain regions, including the motor cortex, basal ganglia, cerebellum, and brainstem. These regions control the intricate muscle movements of the lips, tongue, larynx, and respiratory system necessary for articulating distinct phonemes. The removal or disruption of any of these components would severely impair an individual's ability to generate intelligible speech.
Syntax and Sentence Structure: The syntactic processing of language is primarily associated with the left inferior frontal gyrus (Broca's area) and the left posterior temporal lobe. These regions work in tandem to enable the construction of grammatically correct sentences, following the rules and principles of syntax. Damage to either of these areas can result in agrammatic speech, where sentence structure is severely compromised.
Semantics and Conceptual Understanding: The comprehension of word meanings and their referential relationships is linked to a distributed network in the temporal, parietal, and frontal lobes. This includes areas like the left middle temporal gyrus, involved in lexical-semantic processing, and the angular gyrus, which integrates various sensory inputs to construct conceptual representations. Disrupting this semantic system would undermine an individual's ability to understand the meaning of language.
Pragmatics and Social Communication: The appropriate use of language in social contexts, including understanding non-literal meanings, inferences, and contextual cues, relies on a complex interplay between the prefrontal cortex, temporoparietal junction, and limbic system. These regions are responsible for processing social information, mental states, and pragmatic aspects of language. Impairments in this domain can lead to difficulties in navigating conversational norms and understanding the intended meanings behind utterances.

This interconnectedness of the brain regions and functions underlying language highlights the inherent challenge in reconciling the evolution of language with a gradual, step-wise process. The removal or alteration of any of these critical components would compromise the overall language system, making it difficult to envision how such a complex and integrated faculty could have arisen through a series of small, incremental changes. The level of interdependence and coordination required for effective language use points to the possibility of an intentional, holistic design, rather than a purely accidental, evolutionary development.

The complexity of gene regulation and the interplay between coding and non-coding sequences, epigenetic mechanisms, and developmental processes show that these cannot be adequately explained by incremental evolutionary changes, implying separate origins for humans and chimpanzees.

Moreover, the brain's extraordinary complexity, with its 86 billion neurons and trillions of synaptic connections, cannot be explained as the product of a piecemeal, step-by-step evolutionary process. The intricate integration of various neuronal types, each with their own specialized roles and communication channels, points to an irreducible complexity that defies a gradualistic account.

Around 1,000 enhancer regions exhibit "species-biased" activity, meaning they are more active in one species (human or chimpanzee) compared to the other. Many of these species-biased enhancers and the genes they regulate are known to play crucial roles in craniofacial development and contribute to facial variation within and between species. Specific examples include the genes PAX3 and PAX7, which are expressed at higher levels in chimpanzees and are associated with snout length, shape, and pigmentation. In contrast, the gene BMP4, involved in shaping beaks and jaws in other species, is expressed at higher levels in humans. According to Eric Davidson, it is not possible to evolve one gene regulatory network into another without interrupting it, as these networks are tightly integrated and interdependent systems.

Davidson (2012): No subcircuit functions are redundant with another, and that is why there is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135751/

Therefore, the observed differences in enhancer activities and gene expression patterns between humans and chimpanzees, which are crucial for craniofacial development, are evidence that the gene regulatory networks governing these processes are fundamentally different between the two species. Since it is not possible to gradually evolve one gene regulatory network into another, as outlined by Davidson, then the distinct gene expression patterns governing craniofacial development in humans and chimpanzees are evidence of separate ancestry, rather than a shared evolutionary origin.

Genetic Barriers to Macroevolution: Genetic analysis has also cast doubt on the evolutionary relationship between humans and our supposed ape ancestors. Contrary to the often-cited 99% similarity, more recent studies indicate the human genome may diverge from chimpanzees by as much as 15-20%. Such a significant genetic gap poses a formidable barrier to the macroevolutionary transition from a chimpanzee-like progenitor to modern humans.

Brain Size and Complexity: Homo sapiens generally have larger brains compared to other apes relative to body size. Additionally, the human brain exhibits greater complexity, especially in regions associated with language, abstract thinking, and problem-solving. The prefrontal cortex, in particular, is significantly larger and more developed in humans.

Tool Use and Technology: While some other apes exhibit tool use in the wild, human tool use is far more sophisticated and widespread. Humans have developed complex technologies and cultural practices that allow for the manipulation of the environment in ways that are unparalleled among other primates.

Cultural Complexity: Human societies are characterized by complex social structures, diverse belief systems, and rich cultural traditions. Humans have the ability to create and transmit culture through language, art, music, and ritual, leading to a level of cultural diversity and complexity not observed in other apes.

Bipedalism: Humans are the only apes that habitually walk upright on two legs, a trait known as bipedalism. This unique mode of locomotion frees the hands for tool use and allows for efficient long-distance travel, as well as facilitating the development of complex social structures and the manipulation of the environment.

Extended Childhood and Lifespan: Humans have a longer period of childhood and dependency compared to other apes, allowing for extensive learning, socialization, and cultural transmission. Additionally, humans have a longer lifespan relative to body size compared to other primates.

Symbolic Thought and Abstract Reasoning: Humans possess a capacity for symbolic thought and abstract reasoning that is unparalleled in the animal kingdom. This ability allows for complex problem-solving, planning for the future, and the development of abstract concepts such as mathematics, philosophy, and religion.

Vast genomic differences: The paper highlights numerous differences between the human and chimpanzee genomes, such as chromosomal rearrangements, insertions of transposable elements, deletions, and significant alterations in gene regulation and expression patterns.  The sheer magnitude of these differences is too substantial to have accumulated within the relatively short evolutionary timescale proposed by mainstream science.

Unique genetic elements: Human-specific transposable elements like CpG-SVA and human-specific endogenous retroviral insertions do not have counterparts in the chimpanzee genome. The existence of such uniquely "human" genetic elements is difficult to reconcile with the idea of shared ancestry.


Artistic interpretations and drawings of fossils like Homo erectus and Neanderthals are highly speculative and often depict them as less intelligent than modern humans, despite the fossil evidence suggesting otherwise.The validity of famous fossils touted as evidence of human evolution, such as Lucy and Ardi, raised doubts. For instance, the bones attributed to Lucy may not even belong to the same individual or species, and Ardi's pelvis, initially thought to support upright walking, was found to be more similar to modern apes after extensive digital reconstruction. Fossils that were once hailed as crucial links between apes and humans, such as Ida, have turned out to be misidentified and unrelated to human ancestry, further weakening the fossil evidence. The fossil record appears to consist mainly of two distinct categories: human-like fossils and ape-like fossils, with a significant gap between them, lacking convincing transitional forms that bridge the two groups. Despite ongoing searches, a clear common ancestor between humans and apes has not been found in the fossil record, raising doubts about the proposed evolutionary relationship. Humans possess unique characteristics such as language, mathematics, and a distinct essence or "soul" that sets them apart from animals, implying a separate origin from apes. Fossil evidence for human evolution from apes is weak, riddled with biases, and often based on speculative interpretations rather than solid evidence. The existence of a clear transitional form or common ancestor between humans and apes is doubtful.

The Genesis Account
In contrast, the biblical account of human origins presents a more compelling and coherent narrative. The Genesis creation story describes the intentional formation of Adam, the first man, by God, the ultimate Designer. This framework better explains the remarkable complexity and specified intricacy of the human brain, which bears the hallmarks of intelligent engineering rather than unguided evolutionary processes. The Genesis narrative also aligns with the growing scientific evidence challenging the evolutionary paradigm, such as the improbability of the brain's development and the significant genetic discontinuities between humans and apes. As such, the biblical account of our creation stands as a more plausible and case-adequate explanation for the origins of the human brain and our place in the natural world.

Chimps, our brothers ?  Sem_ty10

https://reasonandscience.catsboard.com

Sponsored content



Back to top  Message [Page 1 of 1]

Permissions in this forum:
You cannot reply to topics in this forum