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Defending the Christian Worldview, Creationism, and Intelligent Design

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, and biodiversity

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Defending the Christian Worldview, Creationism, and Intelligent Design » Theory of evolution » Chimps, our brothers ?

Chimps, our brothers ?

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



Chimps, our brothers ?

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

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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).

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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?

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

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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.

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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.

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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.

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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.
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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)?

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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.

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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.

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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.

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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.
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

The impact of retrotransposons on human genome evolution

Chimps, our brothers ?


Transposons and Retrotransposons

Early Man

Characterization and potential functional significance of human-chimpanzee large INDEL variation

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



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."
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?

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



A Is for . . . Adam or Ape?

Fossil hominin shoulders support an African ape-like last common ancestor of humans and chimpanzees

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



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.

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.


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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.

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.


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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.

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.

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.


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No, I would not believe in something that is impossible.//
-The Y chromosome alone destroys the idea.
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)

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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"

"one finds that the human and chimpanzee genomes are indeed about 95% identical, genome wide"

3-D Human Genome Radically Different from Chimp

A TAD Skeptic: Is 3D Genome Topology Conserved? 13 Nov 2020,

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."

Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content  2013 May 14

Y chromosome shock
More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome and vice versa.

Mitochondrial Eve refuses to die

Eighty percent of proteins are different between humans and chimpanzees

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



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
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.

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



Fazale Rana Yeast Gene Editing Study Raises Questions about the Evolutionary Origin of Human Chromosome 2 September 12, 2018

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.

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