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ElShamah - Reason & Science: Defending ID and the Christian Worldview

Welcome to my library—a curated collection of research and original arguments exploring why I believe Christianity, creationism, and Intelligent Design offer the most compelling explanations for our origins. Otangelo Grasso


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Evolution: Why Darwins theory of evolution does not explain biodiversity

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Why Darwins theory of evolution does not explain biodiversity

https://reasonandscience.catsboard.com/t2623-why-darwins-theory-of-evolution-does-not-explain-biodiversity

Decade-Long Study Challenges Traditional Views of Evolution
By Arizona State UniversitySeptember 15, 2024
https://scitechdaily.com/decade-long-study-challenges-traditional-views-of-evolution/?fbclid=IwY2xjawFU8bhleHRuA2FlbQIxMQABHU_yys1KYjRLP8DffUnjZR63SCFSKmno4H5-sknkMyrYz4dXouBviiI0LA_aem_tcujNBhKh5Y0mOMyQwczUA

Claim: Natural Selection, Genetic Drift, and Gene Flow explain the origin of organismal complexity, and form.
https://www.nature.com/scitable/knowledge/library/natural-selection-genetic-drift-and-gene-flow-15186648/#:~:text=Natural%20selection%2C%20genetic%20drift%2C%20and%20gene%20flow%20are%20the%20mechanisms,Weinberg%20assumptions%2C%20and%20evolution%20occurs.

Reply: The assertion that biodiversity is due to evolution is held on faith by its supporters since the crucial evidence to back up the claim is lacking.

Natural selection is not powerful enough to cause huge change—it is not powerful enough to generate large sections of brand new genetic code (which would be necessary to generate entirely new taxonomic families)

Gene regulatory network co-option is sufficient to induce a morphological novelty in Drosophila:  March 27, 2024
Identifying the molecular origins by which new morphological structures evolve is one of the long-standing problems in evolutionary biology. To date, vanishingly few examples provide a compelling account of how new morphologies were initially formed, thereby limiting our understanding of how diverse forms of life derived their complex features.
https://www.biorxiv.org/content/10.1101/2024.03.22.584840v1

Isn't this confession remarkable?

Gerd B. Müller: Why an extended evolutionary synthesis is necessary 18 August 2017
These examples of conceptual change in various domains of evolutionary biology represent only a condensed segment of the advances made since the inception of the MS theory some 80 years ago. Relatively minor attention has been paid to the fact that many of these concepts, which are in full use today, sometimes contradict or expand central tenets of the MS theory. Given proper attention, these conceptual expansions force us to consider what they mean for our present understanding of evolution. Obviously, several of the cornerstones of the traditional evolutionary framework need to be revised and new components incorporated into a common theoretical structure.
Although today's organismal systems biology is mostly rooted in biophysics and biological function, its endeavors are profoundly integrative, aiming at multiscale and multilevel explanations of organismal properties and their evolution. Instead of chance variation in DNA composition, evolving developmental interactions account for the specificities of phenotypic construction.
https://royalsocietypublishing.org/doi/10.1098/rsfs.2017.0015

Brian R. Johnson (2010): The nature of pattern-formation processes within the cell challenges the traditional view of genetic circuit boards (Kurakin 2005, 2007). According to that view, gene products—structural or enzymatic—do the work within the cell. When thinking about what sorts of genes should evolve and why, one naturally considers genes as acting either independently or in concert with one another. If, however, gene products guide processes already in motion, then the emphasis changes to selection for genes that manipulate and control pattern-formation mechanisms that have their own complex properties. This constrains (at the molecular level) what sort of evolutionary change is possible and also leads to a vision of evolution in which saltatory changes are more important than traditionally thought, as self-organizing mechanisms do not seem to be the products of slow, incremental change.
Brian R. Johnson: Self-organization, Natural Selection, and Evolution: Cellular Hardware and Genetic Software  December 2010

Marta Linde‑Medina On the problem of biological form 5 May 2020
At present, the problem of biological form remains unsolved. Another relevant finding has been the high degree of conservation of developmental genes across taxa. Developmental genes include those encoding transcription factors as well as genes encoding signalling molecules, both of which are involved in gene regulation during embryogenesis. Gene regulation provided an answer to some puzzling results, for example, why species as morphologically diferent as humans and mice nonetheless share 99% of their protein-coding sequences. 
https://sci-hub.ren/10.1007/s12064-020-00317-3

What you believe to be true about evolution, is it true? Or do you just believe that it is true, because you were taught that it is true, but you never looked any further?

NEVER, in over 150 years, since Darwin's book " On the origin of species " was published, has even ONE, amongst hundreds or thousands, if not millions of science papers, provided ONE DEMONSTRATION, and empirical verifiable replicable evidence, that any of the evolutionary mechanisms proposed, could produce a primary macroevolutionary transition zone of speciation and population differentiation.

Simon Conway Morris: Evolutionary Paleobiology at Cambridge, (Runes of Evolution, 38)
argues that adaptation is not an undirected, random walk through all possibilities. For example, when muscle tissue develops into organs that produce electricity, the process requires very precise amino acid replacements at specific sites, together with accelerated evolution of the new function, and Conway Morris concludes that:
“there is little doubt that these changes are very far from random”
He, therefore, argues that while the underlying principles of Darwinian evolution are correct, they do not provide a complete explanation of development, and a more comprehensive theory of evolution is required.

R. DeSalle: Molecular Systematics and Evolution: Theory and Practice 2002
It remains a mystery how the undirected process of mutation, combined with natural selection, has resulted in the creation of thousands of new proteins with extraordinarily diverse and well-optimized functions. This problem is particularly acute for tightly integrated molecular systems that consist of many interacting parts . . . It is not clear how a new function for any protein might be selected for unless the other members of the complex are already present, creating a molecular version of the ancient evolutionary riddle of the chicken and the egg
https://3lib.net/book/2142545/34d7a6

Premise 1: In biosynthesis pathways, proteins are interdependent, meaning they rely on each other for the proper functioning of the pathway.
Premise 2: Interdependence among proteins in biosynthesis pathways indicates a purposeful arrangement to achieve a specific outcome.
Premise 3: A stepwise, evolutionary process would involve the gradual development of biosynthesis pathways, which could require the formation of intermediate protein components.
Premise 4: Many intermediates in an evolutionary process may not have full functionality or may even be nonfunctional.
Conclusion: Therefore, the interdependence of proteins in biosynthesis pathways, along with the presence of potentially nonfunctional intermediates, suggests that a stepwise, evolutionary process is not possible to explain the complex and interdependent nature of these pathways. An intelligent and intentional design is a more plausible explanation for the intricate and functional arrangement observed in biosynthesis pathways.


James A. Shapiro: Evolution: A View from the 21st Century May 18, 2011
It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns of change, and genome sequence studies confirm distinct biases in location of different mobile genetic elements’
https://3lib.net/book/1234158/b6c101

J Baguna: Evo-Devo: the Long and Winding Road  2003
Even to the most unbounded optimist, we are still far from understanding morphological diversity.

Eugene V. Koonin (2010):  The summary of the state of affairs on the 150th anniversary of the Origin is somewhat shocking: in the post-genomic era, all major tenets of the Modern Synthesis are, if not outright overturned, replaced by a new and incomparably more complex vision of the key aspects of evolution. So, not to mince words, the Modern Synthesis is gone. The idea of evolution being driven primarily by infinitesimal heritable changes in the Darwinian tradition has become untenable. 3


Eugene V. Koonin (2012):  Is complexification the prevailing modality of evolution? Phylogenomic reconstruction, at least for bacteria and Archaea, suggests otherwise. It is not surprising that differential gene loss dominates the evolution of commensal bacteria, such as Lactobacilli, from a complex free-living ancestor. A qualitatively similar pattern was detected in evolutionary reconstructions for all bacteria and archaea. Strikingly, more recent reconstructions that were performed using larger genome sets and more sophisticated computational methods confidently indicate that the genome of the last common ancestor of all extant archaea apparently was at least as large and complex as that of typical modern organisms in this domain of cellular life. Fully compatible reconstruction results have been reported for the expanded set of cyanobacterial genomes. Thus, counter-intuitively, at least in prokaryotes, genome shrinkage that is sometimes called streamlining and is attributed to increasing selective pressure in successful, large populations , appears to be is no less and probably more common than genome growth and complexification. 4

Sweeping gene survey reveals new facets of evolution MAY 28, 2018
The most extensive genetics study ever completed the Journal of Human Evolution May, 2018, revealed NO genetic evidence for Evolution. The author, an avid proponent of evolution, was reduced to the following conclusions:
And yet—another unexpected finding from the study—species have very clear genetic boundaries, and there's nothing much in between. "If individuals are stars, then species are galaxies," said Thaler. "They are compact clusters in the vastness of empty sequence space." The absence of "in-between" species is something that also perplexed Darwin, he said.

Perplexed and unexpected? Yes because they so desire proof, yet they can find none. Repeating a lie often may make the lie sound convincing to some, but it does not make it true.
https://phys.org/news/2018-05-gene-survey-reveals-facets-evolution.html

Evolution physical intelligent guiding principle
Numerous scientists have questioned the efficacy of selection and random mutational changes as a mechanism for generating the bio-information necessary for morphological novelty (Eden 1966; Wadington 1968a, b, c; Gould 1982; Yockey 1992, Thomson 1992; Kauffman 1995; Perez 2010; Jorgensen 2007, 2012; Elsheikh 2010, 2014). Eden who was especially concerned about the elements of randomness contended “No currently existing language can tolerate random changes in the symbol sequences which express its sentences. Meaning is almost invariably destroyed. Any changes must be syntactically lawful ones.”

What, if Anything, Is an Evolutionary Novelty? Massimo Pigliucci
The modern synthesis ( of evolution ) provides us with explanatory tools to understand adaptations (natural selection) but falls short when it comes to the question of novelties
http://philpapers.org/archive/PIGWIA/

The origin of the vertebrate skeleton 16 August 2010
No coherent causative model of morphogenesis has ever been presented.
http://journals.cambridge.org/action/displayAbstract;jsessionid=79710AE9A71071921BD4A3CAC34D5C80.journals?aid=7928966&fileId=S147355041000025X

 “Scaling expectations for the time to establishment of complex adaptations”, September 7, 2010, 
“Although the vast majority of research in evolutionary biology is focused on adaption, a general theory for the population-genetic mechanisms by which complex adaptations are acquired remains to be developed.”
http://www.pnas.org/content/early/2010/08/30/1010836107.abstract

“Foundational Concepts: Evolution”
“Scientists are still uncovering the specifics of how, when, and why evolution produced the life we see on Earth today.”
http://www.nmnh.si.edu/paleo/geotime/main/foundation_life3.html

Gene regulatory network architecture in different developmental contexts influences the genetic basis of morphological evolution May 3, 2018
A major goal of biology is to identify the genetic causes of organismal diversity.
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007375

Evolution of Homeobox Gene Clusters in Animals: The Giga-Cluster and Primary vs. Secondary Clustering14 April 2016
There is uncertainty in our understanding of homeobox gene cluster evolution at present. This relates to our still rudimentary understanding of the dynamics of genome rearrangements and evolution over the evolutionary timescales being considered when we compare lineages from across the animal kingdom.
https://www.frontiersin.org/articles/10.3389/fevo.2016.00036/full
My comment: OH NO !!! I can't believe it !! They have no clue? Right. Pro scientists working on the field which try to find out how the instructions of gene expression and repression emerged, admit, they have no idea !!

What’s wrong with evolutionary biology? 20 December 2016
There have been periodic claims that evolutionary biology needs urgent reform. Irrespective of the content of the individual critiques, the sheer volume and persistence of the discontent must be telling us something important about evolutionary biology. Broadly speaking, there are two possibilities, both dispiriting. Either (1) the field is seriously deficient, but it shows a peculiar conservatism and failure to embrace ideas that are new, true and very important; or (2) something about evolutionary biology makes it prone to the championing of ideas that are new but false or unimportant, or true and important, but already well studied under a different branding.
It has been argued here that the discontent is better understood as stemming from a few inescapable properties of living things, which lead to disappointment with evolutionary biology, and a nagging feeling that reform must be overdue. Evolutionary biology, like history, but unlike other natural sciences, raises issues of purpose and agency, alongside those of complexity and generality.
https://link.springer.com/article/10.1007/s10539-016-9557-8?fbclid=IwAR37cKt9BHLC8m4W2YCxYLR9ywLp9Z3-WxSVKm0lPmkEguDYm6MAZvYvTFw

The fundamental theorem of natural selection with mutations 07 November 2017
...THE VAST MAJORITY OF MUTATIONS ARE DELETERIOUS. THIS IS ONE OF THE MOST WELL-ESTABLISHED PRINCIPLES OF EVOLUTIONARY GENETICS, SUPPORTED BY BOTH MOLECULAR AND QUANTITATIVE-GENETIC DATA."
"...a great deal of evidence from several sources strongly suggests that the overall effects of mutations are to REDUCE FITNESS."

Genome-wide analysis of a long-term evolution experiment with Drosophila. 
2010 Sep 15
Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. 6

Evolution by epigenesis: farewell to Darwinism, neo- and otherwise
2004 May-Aug
In the last 25 years, criticism of most theories advanced by Darwin and the neo-Darwinians has increased considerably, and so did their defense. Darwinism has become an ideology, while the most significant theories of Darwin were proven unsupportable. 7
https://www.ncbi.nlm.nih.gov/pubmed/15612191

Dissecting Darwinism
2012 Jan; 25
regarding the origin of the species and life (DNA), even Darwin commented, “If it could be shown that complex systems could not arise by small sequential steps, then my theory would completely break down.” Irreducibly complex systems involving thousands of interrelated specifically coded enzymes do exist in every organ of the human body. At an absolute minimum, the inconceivable self-formation of DNA and the inability to explain the incredible information contained in DNA represent fatal defects in the concept of mutation and natural selection to account for the origin of life and the origin of DNA. As new theories emerge that explain the origin of life, the inevitable emotional accusations of heresy and ignorance are not surprising in a period of scientific revolution. It is therefore time to sharpen the minds of students, biologists, and physicians for the possibility of a new paradigm. 8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246854/

Werner Arber  Nobel Prize in 1978, Physiology or Medicine (sharing the honor with Daniel Nathans and Hamilton O. Smith) for the discovery of restriction enzymes and their application to molecular genetics.
The deeper we penetrate in the studies of genetic exchange the more we discover a multitude of mechanisms" involved in human genetics that falsify the mutation plus natural selection core of macroevolution.
Arber, W, D. Nathans, and H. O. Smith. 1992. 1978 Physiology or Medicine, Nobel Lectures: Physiology or Medicine 1971-1980, 469-492.

James Shapiro Microbiologistof the University of Chicago : 
There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations” (Shapiro 1996).

Lynn Margulis (2003):   Although random mutations influenced the course of evolution, their influence was mainly by loss, alteration, and refinement... Never, however, did that one mutation make a wing, a fruit, a woody stem, or a claw appear. Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity changes shows unambiguous evidence that random mutation itself, even with geographical isolation of populations, leads to speciation. The accumulation of genetic mutations were touted to be enough to change one species to another….No. It wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.
I was taught over and over again that the accumulation of random mutations led to evolutionary change - led to new species. I believed it until I looked for evidence. biology is opening the black box, and demonstrating how organisms develop. We are slowly getting out of a state of ignorance in regard of what mechanisms determines cell shape, assignment of their planes of division, tendencies to move, directions and rates of movement, modes of differentiation into particular cell types, and cell death (apoptosis). The process of morphogenesis, which can be defined as an evolution of the form of an organism, is one of the most intriguing mysteries in the life sciences. The discovery and description of the spatial– temporal distribution of the gene expression pattern during morphogenesis, together with its key regulators, is one of the main recent achievements in developmental biology. Nevertheless, gene expression patterns cannot explain the development of the precise geometry of an organism and its parts in space. 5


Kevin N. Laland: Animal learning as a source of developmental bias 26 August 2019
Learning can influence evolutionary processes in at least two separate ways: either through generating some phenotypic forms more readily than others (a variational bias) or through generating some environmental states more readily than others (a selective bias, a.k.a. “niche construction”).
https://onlinelibrary.wiley.com/doi/abs/10.1111/ede.12311

Based on evidence seen in biochemistry on a molecular level, we can now say affirmatively and conclusively, that Darwin's theory of evolution by natural selection in regards of primary speciation & macroevolutionary level has been falsified.

The selection of random changes of nucleotides being the source of all biological engineering: that claim is nonsense.

Genetic and epigenetic programmed instructional complex codified information and signaling through various signaling pathways on an integrated structural systems-level replace a Darwinian gene-centric view and its various subsequent adaptations, extensions, and new proposals like the modern extended synthesis or the so-called " third way ". The true mechanism is " Biochemical systems programming and signaling", and special creation of species and/or kinds by an intelligent powerful creator. Long periods of time and gradual, evolutionary development is not possible, face the fact that cells and organisms work like gigantic interlocked machines and factory complexes, wherein any case, if one tiny part is missing, nothing goes. Natural selection would not select for components of a complex system that would be useful only in the completion of that much larger system. No glycine amino acids, no pyrimidines, no DNA - no life. No Watson Crick base pair fine-tuning, no DNA - no life. No ribosomal mechanism for amino acid amide bondage, no proteins, no life. No nitrogenase enzymes to fix nitrogen in an energy-demanding, triple bond-breaking process, no ammonia, required to make amino acids - no nitrogen cycle - no advanced life. No chlorophylls, no absorption of light to start photosynthesis, no starch and glucose - cells will have no food supply to sustain complex organisms - no advanced life on earth. No rubisco, no fix of CO2, no hydrocarbons - no advanced life. No counterion in retinal, and rhodopsin could not receive visible light - and there would be no vision on earth by any organism.

A framework for parsing heritable information 22 April 2020
A new framework recasts heredity as a complex, networked information system in which all the regulatory molecules that help the cell to function can constitute a store of hereditary information. Instructions not coded in the DNA are contained in the arrangement of the molecules within cells and their interactions with one another. This arrangement of molecules is preserved and passed down from one generation to the next.  framework recasts inheritance as the combined effects of three components: entities, sensors and properties. Sensors are specific entities that interact with and respond to other entities or to their environment. Sensors respond to certain properties, such as the arrangement of a molecule, its concentration in the cell or its proximity to another molecule. Together, entities, sensors and properties enable a living organism to sense or 'know' things about itself and its environment. Some of this knowledge is used along with the genome in every generation to build an organism. Scientists don't currently have methods to measure some of these things, so this work points to potentially important new avenues for research. 3
http://spaceref.com/news/viewpr.html?pid=55614

Epigenetic Principles of Evolution, 2011, page 19:
The basic tenet of the neo-Darwinian paradigm that changes in genes are responsible for morphological evolution, on which this edifice rises, is not substantiated, hence the empirical foundation of the structure is questionable at best.

If I had to mention ONE word which refutes evolution by mutations and natural selection to explain biological development, body architecture, biodiversity, adaptation, regulation, governing, controlling, recruiting, interpretation, recognition, orchestrating, elaborating strategies, guiding, it would be: SIGNALING. Furthermore the transmission of codified genetic and epigenetic information for development, and adaptation to external cues like food resources and availability, and environmental conditions.

Natural selection cannot induce a design to appear.
And yet, an Aristotelian mythology has been erected, imagining that natural selection creates things. This brings us back to this weekend’s debate, in which evolutionists Lawrence Krauss and Denis Lamoureux propagated and insisted upon this myth, and Stephen Meyer was presented with an enormous unpacking job. How does one disabuse two interlocutors whose perceived success depends on them not understanding the basic facts—in 30 seconds or less? 7

The Biological Big Bang model for the major transitions in evolution
Eugene V Koonin 20 August 2007
Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity.  The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin's original proposal, remains the dominant description of biological evolution.   The cases in point include the origin of complex RNA molecules and protein folds; major groups of viruses; archaea and bacteria, and the principal lineages within each of these prokaryotic domains; eukaryotic supergroups; and animal phyla. In each of these pivotal nexuses in life's history, the principal "types" seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate "grades" or intermediate forms between different types are detectable. Usually, this pattern is attributed to cladogenesis compressed in time, combined with the inevitable erosion of the phylogenetic signal.

A Biological Big Bang (BBB) model is proposed for the major transitions in life's evolution. According to this model, each transition is a BBB such that new classes of biological entities emerge at the end of a rapid phase of evolution (inflation) that is characterized by extensive exchange of genetic information which takes distinct forms for different BBBs.

EVOLUTIONARY BIOSCIENCE AS REGULATORY SYSTEMS BIOLOGY
Eric H. Davidson 2011 Feb 12
The neo-Darwinism ‘erroneously assumes that change in protein coding sequence is the basic cause of change in developmental program; and it erroneously assumes that evolutionary change in body plan morphology occurs by a continuous process. All of these assumptions are basically counterfactual.’ 1

James Shapiro: Microbiologistof the University of Chicago :
There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations” (Shapiro 1996).

Natural selection would not select for components of a complex system that would be useful only in the completion of that much larger system.
In other words : Why would natural selection select an intermediate biosynthesis product, which has by its own no use for the organism, unless that product keeps going through all necessary steps, up to the point to be ready to be assembled in a larger system ? 
A minimal amount of instructional complex information is required for a gene to produce useful proteins. A minimal size of a protein is necessary for it to be functional.   Thus, before a region of DNA contains the requisite information to make useful proteins, natural selection would not select for a positive trait and play no role in guiding its evolution. 

Claim: Evolution is a scientific theory with emphasis on the word “scientific”. It is observable, based on PHYSICAL evidence.
Answer: Evolution by natural selection ( as the mechanism of the origin of species ) is the most successful and widely believed and accepted fairy-tale story ever invented and told, which keeps surviving despite 160 years of scientific advance and discoveries which have falsified the claim. It is able to survive by hiding and disguising behind names as " science', " peer reviewed", " fact", " consensus", and " rational", and because sold and indoctrinated in schools at science classes as credible serious science, endorsed and defended by most specialists like chemists and biologists, and at most universities in the world. Since 90% of the population is gullible and prefer simply to believe others say, they buy the lie, endorse and defend it. Most do not know that there is no consensus about common ancestry. There are critical differences in DNA replication, and the cell membrane, between eukaryotes, and prokaryotes. And mutations in DNA are not determinant of many determinants of body form, shape, and cell differentiation. Epigenetic factors are probably even more relevant than genetic variation to define body form and development.  And with that baggage in their mind, they make the leap of faith and believe, that their "knowledge" makes God superfluous. And so, they can live their lives as pleases, leaving God out of their lives.

The implicit connotation is that when a claim is scientific, it is most probably true since it went through an exhaustive process of peer review and empirical tests. Since evolution as scientific theory stood the test of time, it merits credibility. Science equals to the truth. Since evolution is scientific, it's trustworthy. If the claim is not scientific, it is most probably based on blind faith, and not worth to be taken seriously. For this reason, Darwinists try to discredit Intelligent Design as not being science, but religion. Once they achieve that goal, a further investigation of the scientific facts becomes superfluous.

===============================================================================================================================================

Darwins Theory of  Natural selection has been falsified 
https://reasonandscience.catsboard.com/t2484-darwins-theory-of-natural-selection-has-been-falsified

Op-Ed: Genetic mutations challenges Darwin’s evolution theory
DEC 28, 2012
The death of Darwin's evolution theory continues due to the evidence found in genome deterioration, sickle cell anemia mortality, beneficial mutations elusiveness, disease proliferation, and recent genetic mutations. Analysis of DNA/RNA mutations reveals that these genetic transformations cannot offer meaningful new information in significant quantities. Rather, these mutations will generate information degradation in the genome. 1

Natural Selection Fails to Optimize Mutation Rates for Long-Term Adaptation on Rugged Fitness Landscapes
PEER-REVIEWED September 26, 2008
We allowed mutation rates to evolve, and we evaluated the proximity to the optimum. Although we chose conditions favorable for mutation rate optimization, the evolved rates were invariably far below the optimum across a wide range of experimental parameter settings. We hypothesized that the reason that mutation rates evolved to be suboptimal was the ruggedness of fitness landscapes. We conclude that rugged fitness landscapes can prevent the evolution of mutation rates that are optimal for long-term adaptation. This finding has important implications for applied evolutionary research in both biological and computational realms. 2

Random mutations deteriorate the genome
In a new paper in Science, 3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on the evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.  The abstract said:
Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time. 3

Non-random mutations: How life changes itself: the Read-Write (RW) genome 
And all available scientific evidence also indicates that evolution is an engineered process. In engineering and computer science, evolution never happens by accident. It’s always the result of a deliberate act. A program that can self-evolve is always considered an engineering marvel. 4

Scientists engineer animals with ancient genes to test causes of evolution
January 13, 2017
“For the first test case, we chose a classic example of adaptation-how fruit flies evolved the ability to survive the high alcohol concentrations found in rotting fruit. We found that the accepted wisdom about the molecular causes of the flies’ evolution is simply wrong. 5 Siddiq and Thornton realized that this hypothesis could be tested directly using the new technologies. Siddiq first inferred the sequences of ancient Adh genes from just before and just after D. melanogaster evolved its ethanol tolerance, some two to four million years ago. He synthesized these genes biochemically, expressed them, and used biochemical methods to measure their ability to break down alcohol in a test tube. The results were surprising: the genetic changes that occurred during the evolution of D. melanogaster had no detectable effect on the protein’s function.[/size]

What’s that you say? No detectable effect?

One supposes that the gene selected is one, among very many, that can be best ‘reverse-engineered’ to give a facsimile of the ‘ancient’ form. Yet, when tested in vivo, there is no difference found between the supposed ‘slow’ ancestral gene, and the ‘fast’ extant form. This is not how neo-Darwinism is supposed to work. Something is seriously wrong, no? It might be that the techniques employed to identify the ‘ancestral’ form are bad. Maybe that’s it, and it alone. But, OTOH, maybe something is seriously wrong with current neo-Darwinian theory. Some notions concerning adaptation will, therefore, remain difficult to study rigorously. Nevertheless, because of technical and conceptual advances, it should now be possible to experimentally assess the causal predictions of many previously untested or weakly tested hypotheses of historical molecular adaptation, allowing them to be corroborated or, like the classic hypothesis of ADH divergence in D.melanogaster, decisively refuted. One wonders what’s really left of natural selection. Between Behe’s Edge of Evolution, Shapiro’s “Natural Genetic Engineering,” the whole field of epigenetics, the disappearing of “Junk-DNA”, and now the disappearance of a ‘fitness’ change in a “classic case” of molecular adaptation, can anyone seriously believe that Darwinism has much to say about how life evolves? Remarkably, already in 2010, following paper reported that the claim of NS was not observed in Drosophila. 



Genome-wide analysis of a long-term evolution experiment with Drosophila. 
2010 Sep 15
"Genomic changes caused by epigenetic mechanisms tend to fail to fixate in the population, which reverts back to its initial pattern." That's not all that doesn't fixate. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. 6

Evolution by epigenesis: farewell to Darwinism, neo- and otherwise
2004 May-Aug
In the last 25 years, criticism of most theories advanced by Darwin and the neo-Darwinians has increased considerably, and so did their defense. Darwinism has become an ideology, while the most significant theories of Darwin were proven unsupportable. 7
https://www.ncbi.nlm.nih.gov/pubmed/15612191

Dissecting Darwinism
2012 Jan; 25
regarding the origin of the species and life (DNA), even Darwin commented, “If it could be shown that complex systems could not arise by small sequential steps, then my theory would completely break down.” Irreducibly complex systems involving thousands of interrelated specifically coded enzymes do exist in every organ of the human body. At an absolute minimum, the inconceivable self-formation of DNA and the inability to explain the incredible information contained in DNA represent fatal defects in the concept of mutation and natural selection to account for the origin of life and the origin of DNA. As new theories emerge that explain the origin of life, the inevitable emotional accusations of heresy and ignorance are not surprising in a period of scientific revolution. It is therefore time to sharpen the minds of students, biologists, and physicians for the possibility of a new paradigm. 8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246854/

Werner Arber  Nobel Prize in 1978, Physiology or Medicine (sharing the honor with Daniel Nathans and Hamilton O. Smith) for the discovery of restriction enzymes and their application to molecular genetics.
The deeper we penetrate in the studies of genetic exchange the more we discover a multitude of mechanisms" involved in human genetics that falsify the mutation plus natural selection core of macroevolution.
Arber, W, D. Nathans, and H. O. Smith. 1992. 1978 Physiology or Medicine, Nobel Lectures: Physiology or Medicine 1971-1980, 469-492.

James Shapiro Microbiologistof the University of Chicago : 
There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations” (Shapiro 1996).

Lynn Margulis: 
Although random mutations influenced the course of evolution, their influence was mainly by loss, alteration, and refinement... Never, however, did that one mutation make a wing, a fruit, a woody stem, or a claw appear. Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity changes shows unambiguous evidence that random mutation itself, even with geographical isolation of populations, leads to speciation.
The accumulation of genetic mutations were touted to be enough to change one species to another….No. It wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.
I was taught over and over again that the accumulation of random mutations led to evolutionary change - led to new species. I believed it until I looked for evidence.
biology is opening the black box, and demonstrating how organisms develop. We are slowly getting out of a state of ignorance in regard of what mechanisms determines cell shape, assignment of their planes of division, tendencies to move, directions and rates of movement, modes of differentiation into particular cell types, and cell death (apoptosis).
The process of morphogenesis, which can be defined as an evolution of the form of an organism, is one of the most intriguing mysteries in the life sciences. The discovery and description of the spatial– temporal distribution of the gene expression pattern during morphogenesis, together with its key regulators, is one of the main recent achievements in developmental biology. Nevertheless, gene expression patterns cannot explain the development of the precise geometry of an organism and its parts in space. 1

Steve Meyer: Darwins Doubt, page 136
Randomly cutting and pasting larger blocks of text, as evolutionary biologists often envision, would not make any appreciable difference to the efficacy of a random search of sequence space. Imagine a computer “mutating” at random the text of the play Hamlet either by individual-letter substitutions or by duplicating, swapping, inverting, or recombining whole sections of Shakespeare’s text. Would such a computer simulation have a realistic
chance of generating a completely different and equally informative text such as, say, The Blind Watchmaker by Richard Dawkins, even granting multiple millions of undirected mutational iterations?

===============================================================================================================================================


1. The term 'evolution' is an equivocation fallacy that attempts to define two different proposed processes under the same definition. It is a violation of the logical reasoning process to conclude that the genetic variation we can observe within and around species explains the creation of complex body plans, organs, and other complex systems. Darwin's theory is illogical, serendipitous, and unproven.
2. Complex life by complete accident over billions and trillions of successive serendipitous accidents is an incredulous claim without evidence.
3. Calculations of the time necessary to evolve from goo-to-you reveal such a low probability of macro-evolution happening that the odds are beyond the threshold of 'impossible'. Hitchen's was correct - "What can be asserted without evidence can be dismissed without evidence"...

1. Neo-Darwinism and the Modern Synthesis propose a gene-centric view, a scientific metabiological proposal going back to Darwin's landmark book " On the origin of species " in 1859, where first natural selection was proposed as the mechanism of biodiversity, and later,  gene variation defining how bodies are built and organized.
2. Science researchers have discovered, that robust networks of interactions and biological function, major morphological innovation, development and body form are based on integrative mechanisms, the interplay of genes with the gene regulatory network, Transposons and Retrotransposons, so-called Junk DNA, splicing, and over a dozen epigenetic codes, Membrane targets and patterns, Cytoskeletal arrays, Centrosomes, Ion channels, Sugar molecules on the exterior of cells (the sugar code), that are not specified by nuclear DNA - that is, inheritance is not defined through DNA sequences alone.
3. Science is coming to recognize, that none of the recently proposed alternatives, like the third way, Saltationism, Saltatory ontogeny, mutationism, Genetic drift, or combined theories, do full justice by taking into account all organizational biophysiological hierarchy and complexity which empirical science has come to discover. As such, only a holistic view, namely structuralism,  takes into consideration all influences that form cell form and size, body development and growth, doing justice to the scientific evidence.
4. Scrutinizing which causes ultimately respond for the complexity discovered in life is only satisfying, once the epistemologically flawed foundation of methodological naturalism is taken out of the box, and replaced by a new paradigm, where all possible mechanisms and causal influences are permitted to be scrutinized, investigated, and scientifically tested, including the interaction and creative force of an external intelligent, mental agency outside the known physical world, which through its transcendent power creates, forms and builds all physiobiological lifeforms in all its astounding diversity.

1. Evolution depends on huge ages, billion of years.  Radiometric dating is not reliable.
2. The millions or billions of transitional fossils are missing
3. There is no empirical data of an unorganized undirected unguided Neo-Darwinian accidental random macro-evolutionary event of a change/transition, where  one "kind" did evolve into another beyond the species level (i.e. speciation) ,  like an organism randomly changing/transition into a whole entirely different, new fully functioning biological  organism, the emergence of new complex functions, a new genus or higher rank in taxonomy, with the rise of new body plans
4. Species appear and disappear abruptly in the fossil record.
5. Homo erectus, the precursor of homo sapiens, supposedly populated the earth for 1,5 million years. Where are the millions of fossils that should be buried and be found? They are missing.
6. Most species never changed. We have many animals, like Crocodiles, fish, crabs, insects, that can be found in the fossil record. unchanged.
7. Many fossils have been found with soft tissue, collagen, and proteins, which could not have remained preserved for millions of years.
8. DNA contains a blueprint, an instruction manual to make you, for example. Books, Blueprints, Instruction manuals, information retrieval, transmission, and translation systems do not emerge randomly. They have always an author and can be traced back to an intelligent source.  
9. Machines, assembly lines, computers, recycle systems, error check and repair systems are always invented by intelligence. Biological cells host all this.
10. The information in the genome does not increase but deteriorate.  
11. The human brain is 4 times the size and weight of a Chimp. It is supposed that a common ancestor of Apes and Humans lived 4 million years ago, and from there on, speciation into humans and apes began. The human brain has about 100 billion neurons. That means, there would have had to be the evolution from about 25billion of the common ancestor to 100billion of humans today, or an increase of 75 billion neurons in 4 million years. Or 25 thousand new neurons per year.  Each Neuron has 10 thousand synapses,  which connect to other neurons. Synapses function like a microprocessor and these over ten thousand per neuron would have had to find out how to connect correctly to other neighboring neurons. That is, 25 thousand new neurons, each with 10 thousand synapses, interconnecting correctly, per year !!
12. You cannot change just one body part. In order for evolution to account for the transition of land-living animals, to birds, for example, the whole body plan has to change, and not just single point mutations.
13. Natural selection has been shown to be able to account maximum for two mutations ( malaria ), but for new complex traits to emerge, at least six mutations are required, and it would take too much time to fix them into the population. ( Behe )
14. It has commonly been claimed that the question of how the eye evolved, has been answered. But scientists know this is not true. Rhodopsin is the key enzyme of sight. It is composed of two interdependent parts. Opsin, and retinal. One has no function without the other. And both are finely tuned to interact together. How can evolution explain its origin, if one has no function alone?
An article in Nature magazine confirms :
even as far back as the prokaryotes, the complex seven transmembrane domain arrangement of opsin molecules seems to prevail without simpler photoreceptors existing concurrently. Darwin’s original puzzle over ocular evolution seems still to be with us but now at a molecular level.
15. All complex life forms require interdependent parts. The human eye consists of over two million working parts making it second only to the brain in complexity. The human visual system depends on eye muscles, lubrification, a reliable communications channel (the optic nerve), the data to the central processing unit (the brain) via the visual cortex. If one of these components is missing, no deal. They had to evolve together, but during the evolution process, the single components would confer no survival advantage. What good would an optic nerve be for, without the eye, and the brain?

If someone approaches you, and asks, why is evolution not true, how could we answer in simple terms, without being too technical? I would first outline, that there must be made a differentiation. Darwin's theory has to be subdivided into three main aspects of the theory. 1. Adaptation, the tree of life, where it is claimed, that all life and biodiversity originated from one single ancestor, and macroevolution, and biodiversity which is claimed to be due to macroevolution. The dispute is about common ancestry and macroevolution. Bacteria do not share the same replication process, nor the same cell membrane as animals ( eukaryotes ). Even peer-reviewed science papers admit that, and so, common ancestry of all domains of life is a refuted claim. Most phyla ( animal forms ) appear suddenly in the geological strata, and not gradually, so the fossil record does not support evolution. Macro-evolution has also never been observed in the laboratory. Bacterias can adapt to antibiotics, but will never become something else, then bacteria.   A minimal amount of instructional complex information is required for a gene to produce useful proteins. A minimal size of a protein is necessary for it to be functional.   Thus, before a region of DNA contains the requisite information to make useful proteins, natural selection would not select for a positive trait and play no role in guiding its evolution. Furthermore, organisms on a molecular level are full of molecular machines, Natural selection would not select for components of a complex system that would be useful only in the completion of that much larger system. 1. Complex machines and factories are intelligently designed 2. Biological cells are factories full of complex machines 3. Biological cells are intelligently designed. It has been claimed that so called Junk DNA is evidence of remnants of evolution, and is junk - or, has no function. The design prediction that Junk DNA HAS function is being unraveled, and more and more it is clear, that Junk DNA fullfills life essential functions, like gene regulation ( that is, when a gene is expressed ). Body plan building, and consequently, its supposed evolution, does not depend uniquely on information contained in the genetic code, but beyond ( epigenetics ). That is, what causes body form, and cell size and shape, depends on Membrane targets and patterns, Cytoskeletal arrays, Centrosomes,  cell membrane Ion channels and their location, and  sugar molecules on the exterior of cells (the sugar code), Gene regulatory networks, Transposons and Retrotransposons, and at least on a dozen epigenetic informational codes.

Many individuals who believe in evolution are convinced that there exists an abundance of transitional forms to support evolution. However, what they regard as "transitional" are simply biological similarities between various species or groups, and are not true or actual transitions in Nature. Creationists believe that the biological similarities between various species are due to a common Designer who designed similar functions for similar purposes in all of the various forms of life, from the simplest to the most complex. Evolutionists believe that the biological similarities between species are evidence of common ancestry between all forms of life. Neither position can be scientifically proved.
https://english.pravda.ru/science/106586-evolution_theory/

T.Yonezawa (2012): Some Problems in Proving the Existence of the Universal Common Ancestor of Life on Earth
It seems likely that a huge amount of trials and errors of different forms occurred during the emergence of life and that UCA if existed was just one of them. The probability of survival of life is low unless there are multiple origins.
https://www.hindawi.com/journals/tswj/2012/479824/

Evolution: Charles Darwin was wrong about the tree of life
Genetic tests on bacteria, plants and animals increasingly reveal that different species crossbreed more than originally thought, meaning that instead of genes simply being passed down individual branches of the tree of life, they are also transferred between species on different evolutionary paths. The result is a messier and more tangled "web of life". The findings mean that to link species by Darwin's evolutionary branches is an oversimplification. "The tree of life is being politely buried," said Michael Rose, an evolutionary biologist at the University of California, Irvine.  "What's less accepted is that our whole fundamental view of biology needs to change."
https://www.theguardian.com/science/2009/jan/21/charles-darwin-evolution-species-tree-life




Evolution: Why Darwins theory of evolution does not explain biodiversity OjW7MDV

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135751/

3. Koonin, E.V. (2009). The Origin at 150: is a new evolutionary synthesis in sight? Trends Genet., 25(11), 473–475. Link. (This article reflects on the 150th anniversary of Darwin's "On the Origin of Species" and discusses the potential for a new evolutionary synthesis, considering recent scientific advancements and challenges in the field of evolutionary biology.)
4. Koonin, E.V., & Wolf, Y.I. (2012). Evolution of microbes and viruses: a paradigm shift in evolutionary biology? Front Cell Infect Microbiol., 2: 119. Link. (This article explores the evolutionary dynamics of microbes and viruses, proposing a potential paradigm shift in the field of evolutionary biology by examining how these organisms adapt and evolve, possibly challenging traditional evolutionary theories.)
5. [size=13]Margulis, L., & Sagan, D. (2003). Acquiring Genomes: A Theory Of The Origin Of Species. Link. (In this work, Lynn Margulis and Dorion Sagan present a groundbreaking perspective on species formation, emphasizing the role



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Frank Zindler, President of American Atheists,  in 1996
The most devastating thing though that biology did to Christianity was the discovery of biological evolution. Now that we know that Adam and Eve never were real people the central myth of Christianity is destroyed. If there never was an Adam and Eve there never was an original sin. If there never was an original sin there is no need of salvation. If there is no need of salvation there is no need of a Savior. And I submit that puts Jesus, historical or otherwise, into the ranks of the unemployed. I think that evolution is absolutely the death knell of Christianity.

Reply: The two basic tenets upon which the theory of evolution rests, are the claim of universal common ancestry, and the tree of life. The two claims have been refuted on many grounds. When we talking about the tree of life, we cannot overlook the origin of viruses. Eugene V. Koonin admitted openly in 2020: In the genetic space of viruses and MGEs, no genes are universal or even conserved in the majority of viruses. Viruses have several distinct points of origin, so there has never been a last common ancestor of all viruses. The universal common ancestry of life is also disputed. For example  Eric Bapteste, evolutionary biologist: "We have no evidence at all that the tree of life is a reality." DAVID M. RAUP, paleontologist: Multiple origins of life in the early Precambrian is a reasonable possibility. And C.P. Kempes in the peer-reviewed article: The Multiple Paths to Multiple Life (2021): We argue for multiple forms of life realized through multiple different historical pathways. In regard to the origin of humans: All human beings are 99.9 percent identical in their genetic makeup. Harmful protein-coding mutations in people arose largely in the past 5,000 to 10,000 years. Evidence for a Human Y Chromosome Molecular Clock: Pedigree-Based Mutation Rates Suggest a 4,500-Year History for Human Paternal Inheritance. By comparing the mitochondrial DNA of 147 people from five different ethnic groups, the researchers found that all the individuals analyzed were descendants of the same female lineage, that is, they all had the same original "mother" at the beginning of everything. Thus, they confirmed that all humanity descends from the same woman, who would have been the first Homo sapiens. And they called her "Mitochondrial Eve". These few quotes demonstrate that the major evolutionary tenets are far from being a scientific fact, or consensus among specialists in the field. Adding the complete failure of abiogenesis research permits the inference from eliminative induction:

The most devastating thing though that biology has done to naturalism is the failed claim of chemical and biological evolution. Now that we know that Adam and Eve were real people the central creation narrative of Christianity is confirmed. If there was an Adam and Eve there was an original sin. If there was an original sin there is need of salvation. If there is need of salvation there is need of a Savior. And I submit that puts Jesus, historical or otherwise, into the ranks of the necessary. I think that the failure of abiogenesis and evolution is absolutely the death knell of naturalism.




What is fact :
1. Change over time; history of nature; any sequence of events in nature
2. Changes in the frequencies of alleles in the gene pool of a population
3. Limited common descent: the idea that particular groups of organisms have descended from
a common ancestor.
4. The mechanisms responsible for the change required to produce limited descent with modification; chiefly pre-programmed selection acting on random variations or mutations
5. Natural selection acting up to two random mutations as shown in malaria ( See Behe's Edge of evolution )

What is not fact:
5. Universal common descent: the idea that all organisms have descended from a single common ancestor.
6. Blind watchmaker thesis: the idea that all organisms have descended from common ancestors through unguided, unintelligent, purposeless, material processes such as natural
selection acting on random variations or mutations; the idea that the Darwinian mechanism of natural selection acting on random variation, and other similarly naturalistic mechanisms, completely suffice to explain the origin of novel biological forms and the appearance of design in complex organisms.



Where Do Complex Organisms Come From?
https://reasonandscience.catsboard.com/t2316-where-do-complex-organisms-come-from

Why Darwin was wrong, and what really drives descent with modification
https://reasonandscience.catsboard.com/t2460-what-are-the-mechanisms-that-drive-adaptation-to-the-environment-microevolution-and-secondary-speciation

The tree of life, common descent, common ancestry, a failed hypothesis
https://reasonandscience.catsboard.com/t2239-the-tree-of-life-common-descent-common-ancestry-a-failed-hypothesis

Principal Meanings of Evolution in Biology Textbooks
https://reasonandscience.catsboard.com/t2358-principal-meanings-of-evolution-in-biology-textbooks

Macroevolution. Fact, or fantasy ?
https://reasonandscience.catsboard.com/t1390-macroevolution#1982

Micro evolution and macro evolution  are not the same
https://reasonandscience.catsboard.com/t1641-micro-evolution-and-macro-evolution-are-not-the-same

Failed and falsified evolutionary predictions
https://reasonandscience.catsboard.com/t1666-failed-evolutionary-predictions

Primary, and secondary speciation
https://reasonandscience.catsboard.com/t2360-primary-and-secondary-speciation

Is there evidence for natural selection ?
https://reasonandscience.catsboard.com/t2458-is-there-evidence-for-natural-selection

Eukaryotes evolved from Prokaryotes. Really ?
https://reasonandscience.catsboard.com/t1568-eukaryotes-evolved-from-prokaryotes-really

On the Origin of Mitochondria: Reasons for Skepticism on the Endosymbiotic Story
https://reasonandscience.catsboard.com/t1303-challenges-to-endosymbiotic-theory

Unicellular and multicellular Organisms are best explained through design
https://reasonandscience.catsboard.com/t2010-unicellular-and-multicellular-organisms-are-best-explained-through-design

"Tetrapods evolved" . Really ?  
https://reasonandscience.catsboard.com/t2219-the-evolution-of-tetrapods

What are the mechanisms that drive adaptation to the environment, microevolution, and secondary speciation ?
https://reasonandscience.catsboard.com/t2460-what-are-the-mechanisms-that-drive-adaptation-to-the-environment-microevolution-and-secondary-speciation

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

The origin of Homo Sapiens & timeline of human evolution according to mainstream science.....
https://reasonandscience.catsboard.com/t2596-the-origin-of-homo-sapiens-timeline-of-human-evolution

Chromosome 2, evidence for common ancestry ?
https://reasonandscience.catsboard.com/t1707-chromosome-2




Evolution, adaptation, homeostasis, and the essential preprogrammed processes essential for life to survive in a changing environment 


https://reasonandscience.catsboard.com/t2623-evolution-why-darwins-theory-of-evolution-does-not-explain-biodiversity#5903


Microevolution is better described as adaptation and is an engineered process, which does not happen by accident. The Cell receives macroscopic signals from the environment and responds by adaptive, nonrandom mutations. The capacity of Mammals and other multicellular organisms to adapt to changing environmental conditions is extraordinary.  In order to effectively produce and secrete mature proteins, cellular mechanisms for monitoring the environment are essential. Exposure of cells to various environmental causes accumulation of unfolded proteins and results in the activation of a well-orchestrated set of pathways during a phenomenon known as the unfolded protein response (UPR). Cells have powerful quality control networks consisting of chaperones and proteases that cooperate to monitor the folding states of proteins and to remove misfolded conformers through either refolding or degradation. Free-living organisms, which are more directly exposed to environmental fluctuations, must often survive even harsher folding stresses. These stresses not only disrupt the folding of newly synthesized proteins but can also cause misfolding of already folded proteins.  In living organisms, robustness is provided by homeostatic mechanismsAt least five epigenetic mechanisms are responsible for these life-essential processes :

- heat shock factors (HSFs)
- The unfolded protein response (UPR)
- nonhomologous end-joining and homologous recombination
- The DNA Damage Response
- The Response to Oxidative Stress

The cell modulates the signalling pathways at transcriptional, post-transcriptional and post-translational levels. Complex signalling pathways contribute to the maintenance of systemic homeostasis. Homeostasis is the mechanistic fundament of living organisms. 

Homeostasis, from the Greek words for "same" and "steady," refers to any process that living things use to actively maintain fairly stable conditions necessary for survival. It is also synonymous with robustness and adaptability.

This essential characteristic of living cells, homeostasis, is the ability to maintain a steady and more-or-less constant chemical balance in a changing environment. Cell survival requires appropriate proportions of molecular oxygen and various antioxidants. Reactive products of oxygen, calles Reactive Oxygen Species ( ROS) are amongst the most potent and omnipresent threats faced by cells. Cells, damaged by ROS, irreversibly infected, functionless and/or potentially oncogenic cells are destined for persistent inactivation or elimination, respectively. If mechanisms that do not trigger controlled and programmed Cell death ( apoptosis) are not present at day 1, the organisms cannot survive and dies. Simply put, the principle is that all of a multicellular organism's cells are prepared to suicide when needed for the benefit of the organism as a whole. They eliminate themselves in a very carefully programmed way so as to minimize damage to the larger organism.  On average, in human adults, it’s about 50-70 BILLION cells that die per day. We shed 30,000 to 50,000 skin cells every minute.

1. The control of metabolism is a fundamental requirement for all life, with perturbations of metabolic homeostasis underpinning numerous disease-associated pathologies.
2. Any incomplete Metabolic network without the control mechanisms in place to get homeostasis would mean disease and cell death.
3. A minimal metabolic network and the control mechanisms had to be in place from the beginning, which means, and gradualistic explanation of the origin of biological Cells, and life is unrealistic. 
Life is an all or nothing business and points to a creative act of God.


Following  molecules must stay in a finely tuned order and balance for life to survive:
Halogens like chlorine, fluoride, iodine, and bromine.  The body needs to maintain a delicate balance between all these elements.
Molybdenum (Mo) and iron (Fe) are essential micronutrients required for crucial enzyme activities and mutually impact their homeostasis, which means, they are interdependent on each other to maintain homeostatic levels. 
Potassium plays a key role in maintaining cell function, and it is important in maintaining fluid and electrolyte balance. Potassium-40 is probably the most dangerous light radioactive isotope, yet the one most essential to life. Its abundance must be balanced on a razor’s edge.
The ability of cells to maintain a large gradient of calcium across their outer membrane is universal. All biological cells have a low cytosolic (liquid found inside Cells ) calcium concentration, can and must keep this even when the free calcium outside is up to 20,000 times higher concentrated! 
- Nutrient uptake and homeostasis must be adjusted to the needs of the organisms according to developmental stages and environmental conditions.
Magnesium is the second most abundant cellular cation after potassium. The concentrations are essential to regulate numerous cellular functions and enzymes
Iron is required for the survival of most organisms, including bacteria, plants, and humans. Its homeostasis in mammals must be fine-tuned to avoid iron deficiency with a reduced oxygen transport 
Phosphate, as a cellular energy currency, essentially drives most biochemical reactions defining living organisms, and thus its homeostasis must be tightly regulated. 
Zinc (Zn) is an essential heavy metal that is incorporated into a number of human Zn metalloproteins. Zn plays important roles in nucleic acid metabolism, cell replication, and tissue repair and growth. Zn contributes to intracellular metal homeostasis. 
Selenium homeostasis and antioxidant selenoproteins in the brain: lack of finetuned balance has implications for disorders in the central nervous system
Copper ion homeostasis is maintained through regulated expression of genes involved in copper ion uptake. 

In the early 1960s, Ernest Nagel and Carl Hempel showed that self-regulated systems are teleological.

In his book: THE TINKERER’S ACCOMPLICE, How Design Emerges from Life Itself  J . SCOTT. TURNER, writes at page 12 :

Although I touch upon ID obliquely from time to time, I do so not because I endorse it, but because it is mostly unavoidable. ID theory is essentially warmed-over natural theology, but there is, at its core, a serious point that deserves serious attention. ID theory would like us to believe that some overarching intelligence guides the evolutionary process: to say the least, that is unlikely. Nevertheless, how design arises remains a very real problem in biology.  My thesis is quite simple: organisms are designed not so much because natural selection of particular genes has made them that way, but because agents of homeostasis build them that way. These agents’ modus operandi is to construct environments upon which the precarious and dynamic stability that is homeostasis can be imposed, and design is the result.

My comment: The author does not identify these agents, but Wiki describes agents as CONSCIOUS beings, which act with specific goals in mind. In the case of life, this agent made it possible for biological cells to actively maintain fairly stable levels of various metabolites and molecules, necessary for survival. We are once more, upon careful examination of the evidence in nature, justified to infer an intelligent designer as most case-adequate explanation of the origin of homeostasis and the ability of adaptation, commonly called evolution, of all living organisms.  

Consider the University of California at Berkeley’s “Understanding Evolution” website which informs the student that “natural selection can produce amazing adaptations.” This hilariously appears on a page entitled “Misconceptions about natural selection.”

In fact natural selection, even at its best, does not “produce” anything. Natural selection does not and cannot influence the construction of any adaptations, amazing or not. If a mutation occurs which improves differential reproduction, then it propagates into future generations. Natural selection is simply the name given to that process. It selects for survival of that which already exists. Natural selection has no role in the mutation event. It does not induce mutations, helpful or otherwise, to occur. According to evolutionary theory every single mutation, leading to every single species, is a random event with respect to need.

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the most extensive genetics study ever completed the Journal of Human Evolution May, 2018, revealed NO genetic evidence for Evolution. The author, an avid Evolutionist, was reduced to the following conclusions:
And yet—another unexpected finding from the study—species have very clear genetic boundaries, and there's nothing much in between.
"If individuals are stars, then species are galaxies," said Thaler. "They are compact clusters in the vastness of empty sequence space."
The absence of "in-between" species is something that also perplexed Darwin, he said.

Perplexed and unexpected? Yes because they so desire proof, yet they can find none.
Repeating a lie often may make the lie sound convincing to some, but it does not make it true.
https://phys.org/news/2018-05-gene-survey-reveals-facets-evolution.html


Numerous scientists have questioned the efficacy of selection and random mutational changes as a mechanism for generating the bio-information necessary for morphological novelty (Eden 1966; Wadington 1968a, b, c; Gould 1982; Yockey 1992, Thomson 1992; Kauffman 1995; Perez 2010; Jorgensen 2007, 2012; Elsheikh 2010, 2014).[/size]
https://link.springer.com/article/10.1007/s40974-016-0010-2

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Behe, the edge of evolution

Recall the example of sickle cell disease. The sickle cell mutation is both a life saver and a life destroyer. It fends off malaria, but can lead to sickle cell disease. However,hemoglobin C-Harlem has all the benefits of sickle, but none of its fatal drawbacks. So in western and central Africa, a population of humans that had normal hemoglobin would be worst off, a population that had half normal and half sickle would be better off, and a population that had half normal and half C-Harlem would be best of all. But if that’s the case, why bother with sickle hemoglobin? Why shouldn’t evolution just go from the worst to the best case directly? Why not just produce the C-Harlem mutation straightaway and avoid all the misery of sickle? The problem with going straight from normal hemoglobin to hemoglobin C-Harlem is that, rather than walking smoothly up the stairs, evolution would have to jump a step. C-Harlem differs from normal hemoglobin by two amino acids. In order to go straight from regular hemoglobin to C-Harlem, the right mutations would have to show up simultaneously in positions 6 and 73 of the beta chain of hemoglobin. Why is that so hard? Switching those two amino acids at the same time would be very difficult for the same reason that developing resistance to a cocktail of drugs is difficult for malaria—the odds against getting two needed steps at once are the multiple of the odds for each step happening on its own. What are those odds? Very low. The human genome is composed of over three billion nucleotides. Yet only a hundred million nucleotides seem to be critical, coding for proteins or necessary control features. The mutation rate in humans (and many other species) is around this same number; that is, approximately one in a hundred million nucleotides is changed in a baby compared to its parents (in other words, a total of about thirty changes per generation in the baby’s three-billion-nucleotide genome, one of which might be in coding or control regions). In order to get the sickle mutation, we can’t change just any nucleotide in human DNA; the change has to occur at exactly the right spot. So the probability that one of those mutations will be in the right place is one out of a hundred million. Put another way, only one out of every hundred million babies is born with a new mutation that gives it sickle hemoglobin. Over a hundred generations in a population of a million people, we would expect the mutation to occur once by chance. That’s within the range of what can be done by mutation/selection.

To get hemoglobin C-Harlem, in addition to the sickle mutation we have to get the other mutation in the beta chain, the one at position 73. The odds of getting the second mutation in exactly the right spot are again about one in a hundred million. So the odds of getting both mutations right, to give hemoglobin C Harlem in one generation in an individual whose parents have normal hemoglobin, are about a hundred million times a hundred million (10^16). On average, then, nature needs about that many babies in order to find just one that has the right double mutation. With a generation time of ten years and an average population size of a million people, on average it should take about a hundred billion years for that particular mutation to arise—more than the age of the universe.

Hemoglobin C-Harlem would be advantageous if it were widespread in Africa, but it isn’t. It was discovered in a single family in the United States, where it doesn’t offer any protection against malaria for the simple reason that malaria has been eradicated in North America. Natural selection, therefore, may not select the mutation, and it may easily disappear by happenstance if the members of the family don’t have children, or if the family’s children don’t inherit a copy of the C-Harlem gene. It’s well known to evolutionary biologists that the majority even of helpful mutations are lost by chance before they get an opportunity to spread in the population. If that happens with C-Harlem, we may have to wait for another hundred million carriers of the sickle gene to be born before another new C-Harlem mutation arises.

============================================================================================================================================

Satan and his demons must have held a long-standing debate to solve the problem of emerging evidence of design by the new arising disciplines of science, and scientific discoveries of the 19th century, and the writings of great minds like Paley. He needed urgently an effective, long lasting, damage limiting counter-idea and ways to infuse his devilishly fashioned sciency sounding elaborations long-term to people.

So he inspired Charles Darwin et al to come up with his pseudo-scientific nonsense but fashioned in a way which is the imprint of masters: The lies were hidden so well, that even after hundreds of years, the poor human mind is blinded by it.

The prudish costumes in the English empires were put away without a heavy conscience since Darwin's idea supposedly made God superfluous, and mistresses had their heydays. Past the first impact, his idea strengthened and survived in the academia, because the scientific evidence to dismask the lies came only long afterward.

In regard of the origin of life, in a now famous paragraph in the letter sent on February 1st, 1871, Darwin stated that

«it is often said that all the conditions for the first production of a living being are now present, which could ever have been present. But if (and oh what a big if) we could conceive in some warm little pond with all sort of ammonia and phosphoric salts,—light, heat, electricity present, that a protein compound was chemically formed, ready to undergo still more complex changes, at the present such matter would be instantly devoured, or absorbed, which would not have been the case before living creatures were formed [...]».
~Charles Darwin, in a letter to Joseph Hooker (1871)

What unraveled in front of our eyes along the last decades, however, is a new world of exquisite complexity, sophisticated engineering, factory-like production lines, storage, transmission and use of an enormous amount of genetic and epigenetic information, molecular highways and so on.

In the same sense, as Charly was considerably wrong in regard to the complexity of biological cells out of the ignorance of his days, he was in regard of the true mechanisms that define body form, cell shape, and biodiversity, and the extent and range of natural selection ( which is limited to just 2 mutations ).

But the father of lies has mastered it, to keep the lie alive, the claim of the superpowers of evolution walking around like a Zombie, and keeping the effects of this mental nuclear bomb: Many reject God by deluding themselves, by believing that evolution is the better answer to origins, and settles the issue. Same as the illuster genitors, 150 years ago. The crutches of evolution keep doing their job.

Once the crutches of evolution will be laid down, once for all, it will be much too late, anyway. Sadly.



Evolution: Why Darwins theory of evolution does not explain biodiversity LKfFNY4



Last edited by Otangelo on Mon Sep 16, 2024 5:13 am; edited 9 times in total

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A proof or disproof is a kind of a transaction. There is no such thing as absolutely proving or disproving something; there is only such a thing as proving or disproving something to SOMEBODY'S satisfaction. If the party of the second part is too thick or too ideologically committed to some other way of viewing reality, then the best proof in the world will fall flat and fail.

In the case of evolution, what you have is a theory which has been repeatedly and overwhelmingly disproved over a period of many decades now via a number of independent lines reasoning and yet the adherents go on with it as if nothing had happened and, in fact, demand that the doctrine be taught in public schools at public expense and that no other theory of origins even ever be mentioned in public schools, and attempt to enforce all of that via political power plays and lawsuits.

At that point, it is clear enough that no disproof or combination of disproofs would ever suffice, that the doctrine is in fact unfalsifiable and that Carl popper's criteria for a pseudoscience is in fact met.

Once again for anybody who may have missed this earlier:

The educated lay person is not aware of how overwhelmingly evolution has been debunked over the last century.

The following is a minimal list of entire categories of evidence disproving evolution:

The decades-long experiments with fruit flies beginning in the early 1900s. Those tests were intended to demonstrate macroevolution; the failure of those tests was so unambiguous that a number of prominent scientists disavowed evolution at the time.

The discovery of the DNA/RNA info codes (information codes do not just sort of happen...)

The fact that the info code explained the failure of the fruit-fly experiments (the whole thing is driven by information and the only info there ever was in that picture was the info for a fruit fly...)

The discovery of bio-electrical machinery within 1-celled animals.

The question of irreducible complexity.

The Haldane Dilemma. That is, the gigantic spaces of time it would take to spread any genetic change through an entire herd of animals.

The increasingly massive evidence of a recent age for dinosaurs. This includes soft tissue being found in dinosaur remains, good radiocarbon dates for dinosaur remains (blind tests at the University of Georgia's dating lab), and native American petroglyphs clearly showing known dinosaur types.

The fact that the Haldane dilemma and the recent findings related to dinosaurs amount to a sort of a time sandwich (evolutionites need quadrillions of years and only have a few tens of thousands).

The dna analysis eliminating neanderthals and thus all other hominids as plausible human ancestors.

The total lack of intermediate fossils where the theory demands that the bulk of all fossils be clear intermediate types. "Punctuated Equilibria" in fact amounts to an attempt to get around both the Haldane dilemma and the lack of intermediate fossils, but has an entirely new set of overwhelming problems of its own...

The question of genetic entropy.

The obvious evidence of design in nature.

The arguments arising from pure probability and combinatoric considerations.

Here's what I mean when I use the term "combinatoric considerations"...

The best illustration of how stupid evolutionism really is involves trying to become some totally new animal with new organs, a new basic plan for existence, and new requirements for integration between both old and new organs.

Take flying birds for example; suppose you aren't one, and you want to become one. You'll need a baker's dozen highly specialized systems, including wings, flight feathers, the specialized system which allows flight feathers to pivot so as to open on upstrokes and close to trap air on downstrokes (like a venetian blind), a specialized light bone structure, specialized flow-through design heart and lungs, specialized tail, specialized general balance parameters etc.

For starters, every one of these things would be antifunctional until the day on which the whole thing came together, so that the chances of evolving any of these things by any process resembling evolution (mutations plus selection) would amount to an infinitessimal, i.e. one divided by some gigantic number.

In probability theory, to compute the probability of two things happening at once, you multiply the probabilities together. That says that the likelihood of all these things ever happening, best case, is ten or twelve such infinitessimals multiplied together, i.e. a tenth or twelth-order infinitessimal. The whole history of the universe isn't long enough for that to happen once.

All of that was the best case. In real life, it's even worse than that. In real life, natural selection could not plausibly select for hoped-for functionality, which is what would be required in order to evolve flight feathers on something which could not fly apriori. In real life, all you'd ever get would some sort of a random walk around some starting point, rather than the unidircetional march towards a future requirement which evolution requires.

And the real killer, i.e. the thing which simply kills evolutionism dead, is the following consideration: In real life, assuming you were to somehow miraculously evolve the first feature you'd need to become a flying bird, then by the time another 10,000 generations rolled around and you evolved the second such reature, the first, having been disfunctional/antifunctional all the while, would have DE-EVOLVED and either disappeared altogether or become vestigial.

Now, it would be miraculous if, given all the above, some new kind of complex creature with new organs and a new basic plan for life had ever evolved ONCE.

Evolutionism, however (the Theory of Evolution) requires that this has happened countless billions of times, i.e. an essentially infinite number of absolutely zero probability events.

I ask you: What could be stupider than that?

Fruit flies breed new generations every few days. Running a continuous decades-long experiment on fruit flies will involve more generations of fruit flies than there have ever been of anything resembling humans on Earth. Evolution is supposed to be driven by random mutation and natural selection; they subjected those flies to everything in the world known to cause mutations and recombined the mutants every possible way, and all they ever got was fruit flies.

Richard Goldschmidt wrote the results of all of that up in 1940, noting that it was then obvious enough that no combination of mutation and selection could ever produce a new kind of animal.

There is no excuse for evolution to ever have been taught in schools after 1940.  Credito to: Theodore Holden

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1: Lamarkian Inheritance

2: Spontaneous Generation
3: Pangenesis
4: Darwin Theory of Evolution
5: Neo Darwin evolution
6: Synthetic Theory
7: Saltation
8. Punctuated Equilibrium evolution
9. Divergent /Convergent Evolution
10: Parallel Evolution
11: Preadaptive Evolution
12. Reductive evolution
13: The Third Way or the Extended Evolutionary Synthesis EES
14: Recapitulation Theory
15: Self assembly or self organisation/Plasticity
16: Biochemical predestination
17: Maximum Entropy Production (MEP),
18: Population Dynamics,
19: Facilitated Variation,
20: Semi-Meiosis,
21: Niche Construction,
22: Metabolic Rate Theory
23: Zoogenesis
24: Orthogenesis
25: Pangenesis
26: Gaia Theory
27: Evo-Devo
28: Symbiogenesis
29: Panspermia
30: Undirected Panspermia
31: Necropanspermia
32: Rapid Evolution
33: Moderm Evolution Synthesis
34: Cladogenesis/Anagenesis
35: The MacCready Explosion
36: Sympatric speciation
37: Co-option evolution
38: Reticulate evolution
39: The MFAP hypothesis (youll love this one)
40: Super Evolution - where 10 million stars formed every minute for 13.7 billion years WOW.
41: Escape from Adaptive Conflict (EAC)
41: Reserved for the next evo term just for my mate Bill Ludlow
42: (Insert anything you like here) General theory of evolution or maybe Special theory of evolution or .... why not go for it ------> The Theory of Everything or Anything?
43: Out of context Theory - evos accuse us that we don't understand the "word usage" of Darwins time and we take him out if context.
Manage

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Science is ignorant in regard to how evolution supposedly works

https://reasonandscience.catsboard.com/t1826-it-s-not-known-and-mainstream-science-is-ignorant-in-regard-of-how-evolution-supposedly-works

There is no publication in the scientific literature – in prestigious journals, specialty journals, or books – that describes how molecular evolution of any real, complex, biochemical system either did occur or even might have occurred. There are assertions that such evolution occurred, but absolutely none is supported by pertinent experiments or calculations… despite comparing sequences and mathematical modeling, molecular evolution has never addressed the question of how complex structures came to be.

EVEN PROPONENTS OF EVOLUTION ADMIT TO NOT KNOWING HOW EVOLUTION SUPPOSEDLY WORKS:

The modern synthesis ( of evolution ) provides us with explanatory tools to understand adaptations (natural selection) but falls short when it comes to the question of novelties
http://philpapers.org/archive/PIGWIA/

No coherent causative model of morphogenesis has ever been presented.
http://journals.cambridge.org/action/displayAbstract;jsessionid=79710AE9A71071921BD4A3CAC34D5C80.journals?aid=7928966&fileId=S147355041000025X

“Although the vast majority of research in evolutionary biology is focused on adaption, a general theory for the population-genetic mechanisms by which complex adaptations are acquired remains to be developed.”
Proceedings of the National Academy of Sciences of the U.S., “Scaling expectations for the time to establishment of complex adaptations”, September 7, 2010, doi:10.1073/pnas.1010836107.
http://www.pnas.org/content/early/2010/08/30/1010836107.abstract

“Students should realize that although virtually all scientists accept the general concept of evolution of species, scientists do have different opinions on how fast and by what mechanisms evolution proceeds.”
The American Association for the Advancement of Science, Educational Benchmarks, (F) Evolution of Life
http://www.project2061.org/publications/bsl/online/ch5/ch5.htm#F

“Scientists are still uncovering the specifics of how, when, and why evolution produced the life we see on Earth today.”
Smithsonian’s National Museum of Natural History’s website, “Foundational Concepts: Evolution” page
http://www.nmnh.si.edu/paleo/geotime/main/foundation_life3.html

“But they are trying to figure out how evolution happens, and that’s not an easy job.”
University of California Museum of Paleontology and the National Center for Science Education
http://evolution.berkeley.edu/evolibrary/article/0_0_0/evo_50

“Much of the recent experimental work on natural selection has focused on three goals: determining how common it is, identifying the precise genetic changes that give rise to the adaptations produced by natural selection, and assessing just how big a role natural selection plays in a key problem of evolutionary biology—the origin of new species.”
Scientific American Magazine, “The Evolution of Evolution: Testing Natural Selection with Genetics”, December 18, 2008.
http://www.sciam.com/article.cfm?id=testing-natural-selection&print=true

A major goal of biology is to identify the genetic causes of organismal diversity.
May 3, 2018
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007375

Evolution as fact and theory
https://en.wikipedia.org/wiki/Evolution_as_fact_and_theory
Other commentators – focusing on the changes in species over generations and in some cases common ancestry – have stressed, in order to emphasize the weight of supporting evidence, that evolution is a fact, arguing that the use of the term "theory" is not useful:

Richard Lewontin wrote, "It is time for students of the evolutionary process, especially those who have been misquoted and used by the creationists, to state clearly that evolution is fact, not theory."

Douglas J. Futuyma writes in Evolutionary Biology (1998), "The statement that organisms have descended with modifications from common ancestors—the historical reality of evolution—is not a theory. It is a fact, as fully as the fact of the earth's revolution about the sun."

Richard Dawkins says, "One thing all real scientists agree upon is the fact of evolution itself. It is a fact that we are cousins of gorillas, kangaroos, starfish, and bacteria. Evolution is as much a fact as the heat of the sun. It is not a theory, and for pity's sake, let's stop confusing the philosophically naive by calling it so. Evolution is a fact."

Neil Campbell wrote in his 1990 biology textbook, "Today, nearly all biologists acknowledge that evolution is a fact. The term theory is no longer appropriate except when referring to the various models that attempt to explain how life evolves... it is important to understand that the current questions about how life evolves in no way implies any disagreement over the fact of evolution."

Evolution, theory in biology postulating that the various types of plants, animals, and other living things on Earth have their origin in other preexisting types and that the distinguishable differences are due to modifications in successive generations. The theory of evolution is one of the fundamental keystones of modern biological theory. Evolutionists no longer are concerned with obtaining evidence to support the fact of evolution but rather are concerned with what sorts of knowledge can be obtained from different sources of evidence.
https://www.britannica.com/science/evolution-scientific-theory

Can you see the contradiction?

More:
Why Darwins theory of evolution does not explain biodiversity

https://reasonandscience.catsboard.com/t2623-why-darwins-theory-of-evolution-does-not-explain-biodiversity

What is fact :
1. Change over time; history of nature; any sequence of events in nature
2. Changes in the frequencies of alleles in the gene pool of a population
3. Limited common descent: the idea that particular groups of organisms have descended from
a common ancestor.
4. The mechanisms responsible for the change required to produce limited descent with modification; chiefly pre-programmed selection acting on random variations or mutations
5. Natural selection acting up to two random mutations as shown in malaria ( See Behe's Edge of evolution )

What is not fact:
5. Universal common descent: the idea that all organisms have descended from a single common ancestor.
6. Blind watchmaker thesis: the idea that all organisms have descended from common ancestors through unguided, unintelligent, purposeless, material processes such as natural
selection acting on random variations or mutations; the idea that the Darwinian mechanism of natural selection acting on random variation, and other similarly naturalistic mechanisms, completely suffice to explain the origin of novel biological forms and the appearance of design in complex organisms.

Evolution: Why Darwins theory of evolution does not explain biodiversity Quote-10

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1: Lamarkian Inheritance
2: Spontaneous Generation
3: Pangenesis
4: Darwin Theory of Evolution
5: Neo Darwin evolution
6: Synthetic Theory
7: Saltation
8. Punctuated Equilibrium/Explosive evolution
9: Maintenance evolution
10: Switch evolution
11: Forked speciation
12: Divergent /Convergent Evolution
13: Parallel Evolution
14: Preadaptive Evolution
15. Reductive evolution
16: The Third Way or the Extended Evolutionary Synthesis EES
17: Recapitulation Theory
18: Self assembly or self organisation/Plasticity
19: Biochemical predestination
20: Maximum Entropy Production (MEP),
21: Population Dynamics,
22: Facilitated Variation,
23: Semi-Meiosis,
24: Niche Construction,
25: Metabolic Rate Theory
26: Zoogenesis
27: Orthogenesis
28: Pangenesis
29: Gaia Theory
30: Evo-Devo
31: Symbiogenesis
32: Panspermia
33: Undirected Panspermia
34: Necropanspermia
35: Rapid Evolution
36: Moderm Evolution Synthesis
37: Cladogenesis/Anagenesis
38: The MacCready Explosion
39: Sympatric speciation
40: Co-option evolution
41: Reticulate evolution
42: The MFAP hypothesis (youll love this one)
43: Super Evolution - where 10 million stars formed every minute for 13.7 billion years WOW.
44: Escape from Adaptive Conflict (EAC)
45: Schrodingers Quantum Theory of Mutation
46: Out of context Theory - evos accuse us that we don't understand the "word usage" of Darwins time and we take him out if context.
47: Evolution is a Markov Chain, by Keith Fosberg from FB
48: Reserved for the next evo term just for my mate Bill Ludlow
49: (Insert anything you like here) General theory of evolution or maybe Special theory of evolution or .... why not go for it ------> The Theory of Everything or Anything?

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" Creationists have no clue how evolution works " Is it? Who has?

https://reasonandscience.catsboard.com/t2623-evolution-why-darwins-theory-of-evolution-does-not-explain-biodiversity#6260

One of the often heard rebuttals of atheists which use evolution as crutches to back up their views that God is not required is:

" You don't know how evolution works".

This demonstrates that:

They do think they know how evolution works. and that they, in reality, have NO CLUE what they are talking about.

In the same sense, as on top of making complex factories, first  is the elaboration of a master plan, a general layout of an industrial complex of various interlinked factory buildings, and below are the blueprints to make the individual factories, compartments, assembly lines, machines, robots, machine elements, basic building blocks, material specification, etc.
in biology, there is as well a master plan, which outlines the entire structure and body architecture of an organism. That master plan is stored in the genome, in a section, called homeobox.

Homeobox genes are a large family of similar genes that direct the formation of many body structures during early embryonic development. A homeobox is a DNA sequence found within genes that are involved in the regulation of patterns of anatomical development morphogenesis in animals, fungi, and plants. In humans, the homeobox gene family contains an estimated 235 functional genes and 65 pseudogenes, which are structurally similar genes that do not provide instructions for making proteins. Homeobox genes are present on every human chromosome, and they often appear in clusters. Many classes and subfamilies of homeobox genes have been described, although these groupings are used inconsistently.

Homeoboxes have been found in fungi, plants and animals. In each "kingdom" homeobox genes occupy a key position in the genetic control of either cell differentiation, morphogenesis and or body plan specification.

The degree of sequence conservation of the homeodomain is extremely high indicating strong functional constraints leading to a high pressure to retain the homeobox sequences constant.

Single mutations in HOXA1 sequence, is crucial in the determination of severe cardiovascular malformations. Mice knock out for Hoxa1, show defects as interrupted aortic arch, aberrant subclavian artery and Tetralogy of Fallot. Hoxa1 play a key role in the arrangement of the great arteries and heart outflow tract.

Mice knockout for Hoxa3 gene, show cardiac abnormalities and links between circulatory and respiratory systems. The HOXC5, HOXA5 and HOXB5 expression, induce a development of new pharyngeal arches containing a new aortic arch artery with regular flow. HOXC9 is overexpressed, in human smooth muscle cells and the cardiovascular system during embryogenesis.

What does that demonstrate?  In a vast gene sequence space, functional Gene regulatory sequences, Master genes that direct body development, are under severe constraint, and only very specific homeobox sequences are functional, and even A SINGLE MUTATION has catastrophic consequences.

SORRY, Charly, but once again, your ideas are being refuted and falsified. Sad that you are not here to clean up the mess you left, and so many still believe in your unproven claims, nothing else than guesswork, which is driving so many away from the MASTER, that invented all this stuff.

So. What does science say to this ?? Lets see.

Evolution of Homeobox Gene Clusters in Animals: The Giga-Cluster and Primary vs. Secondary Clustering

https://www.frontiersin.org/articles/10.3389/fevo.2016.00036/full

There is uncertainty in our understanding of homeobox gene cluster evolution at present. This relates to our still rudimentary understanding of the dynamics of genome rearrangements and evolution over the evolutionary timescales being considered when we compare lineages from across the animal kingdom.

OH NO !!! I can't believe it !! They have no clue? Right. Pro scientists working on the field which try to find out how the instructions of gene expression and repression emerged, admit, they have no idea !!

Well, they are at least honest to admit the situation.

But the ultracrepidarian " i know it better " experts we deal with on FB feel themselves in the position to tell us the Levites, and educate us on evolutionary developmental biology. We, creationists, are the don't know ists and ignorantes, who do have no clue how evolution works... HÁ !!



Last edited by Otangelo on Wed Jan 05, 2022 7:57 am; edited 1 time in total

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Do mutations of developmental control genes explain body plan diversity? 

It appears that changes in the spatial regulation of developmental control genes are related to morphological divergence, suggesting that the changes in morphology are the result of nucleotide substitutions in cis-regulatory elements and amino-acid substitutions in transcription factors affecting the regulation of gene expression. This notion is not new and was hypothesized more than four decades ago by Britten and Davidson (1969, 1971), who postulated that intergenic genomic regions and mutational changes in protein-coding sequences have an important role in determining differences in gene regulatory patterns, and consequently, in animal body plan diversity. Therefore, animal body plan evolution, along with cell type evolution, is controlled by the precise regulation of gene expression in time and space, which in turn is driven by developmental gene regulatory networks (dGRNs). Changes in animal body plan forms are the result of evolutionary changes in the architecture of these dGRNs. The evolution of dGRNs plays a key role in the emergence of animal diversity. 1

We feel that, generally, the appearance of new structural (producer) genes represents a minor part of the changes involved. A sort of syllogism highlights this view:

metazoan organization arises through cellular ontogeny; 
ontogeny results from the operation of genetic regulatory programs; major events in metazoan evolution consist of changes in organization; thus 
the understanding of major events in evolution requires the examination of the origin of novel programs of gene regulation. 2 

1. http://sci-hub.tw/https://academic.oup.com/icb/article-abstract/58/4/640/5039865?redirectedFrom=fulltext

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Adaptation of cells to new environments

https://reasonandscience.catsboard.com/t2061p125-my-articles#6174

Several life-essential EPIGENETIC mechanisms respond to environmental stress. 

- heat shock factors (HSFs)
- The unfolded protein response (UPR)
- nonhomologous end-joining and homologous recombination
- The DNA Damage Response
- The Response to Oxidative Stress

Evolution takes supposedly thousands of years to gain an environmental advantage. So what environmental benefit would evolution supposedly provide, if adapting and responding to environmental stimuli is not only a life-essential process which had to be fully implemented when life began but, furthermore, a pre-programmed process based on information through signaling networks?


Cells have many mechanisms to modulate the signaling pathways at transcriptional, post-transcriptional and post-translational levels. 

Organisms respond to short-term environmental changes by reversibly adjusting their physiology to maximize resource utilization while maintaining structural and genetic integrity by repairing and minimizing damage to cellular infrastructure, thereby balancing innovation with robustness. The cell’s initial response to a stressful stimulus is geared towards helping the cell to defend against and recover from the insult. 2 The fact that the cell’s survival critically depends on the ability to mount an appropriate response towards environmental or intracellular stress stimuli can explain why this reaction is highly conserved in evolution. The adaptive capacity of a cell ultimately determines its fate.

One of the reasons behind the evolutionary success of mammals (and other multicellular organisms) is their extraordinary capacity to adapt to changing environmental conditions. 3

Maybe the author should ask himself, how the Cell could have survived without the mechanism implemented from day one !!


Evolution: Why Darwins theory of evolution does not explain biodiversity Eo1nbw10

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Simulating evolution by gene duplication of protein features that require multiple amino acid residues

Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function. Models of the process often implicitly assume that a single mutation to the duplicated gene can confer a new selectable property. Yet some protein features, such as disulfide bonds or ligand binding sites, require the participation of two or more amino acid residues, which could require several mutations. Here we model the evolution of such protein features by what we consider to be the conceptually simplest route—point mutation in duplicated genes. We show that for very large population sizes N, where at steady state in the absence of selection the population would be expected to contain one or more duplicated alleles coding for the feature, the time to fixation in the population hovers near the inverse of the point mutation rate, and varies sluggishly with the λth root of 1/N, where λ is the number of nucleotide positions that must be mutated to produce the feature. At smaller population sizes, the time to fixation varies linearly with 1/N and exceeds the inverse of the point mutation rate. We conclude that, in general, to be fixed in 10^8 generations, the production of novel protein features that require the participation of two or more amino acid residues simply by multiple point mutations in duplicated genes would entail population sizes of no less than 10^9.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2286568/?fbclid=IwAR0B7XJ-S9yuXR69VDGB_HE7_9OipiuBopYt5az6bqu7gn2ZvDXgCzHhMdY

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11Evolution: Why Darwins theory of evolution does not explain biodiversity Empty What’s wrong with evolutionary biology? Thu Dec 20, 2018 9:13 am

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What’s wrong with evolutionary biology?

There have been periodic claims that evolutionary biology needs urgent reform. Irrespective of the content of the individual critiques, the sheer volume and persistence of the discontent must be telling us something important about evolutionary biology. Broadly speaking, there are two possibilities, both dispiriting. Either (1) the field is seriously deficient, but it shows a peculiar conservatism and failure to embrace ideas that are new, true and very important; or (2) something about evolutionary biology makes it prone to the championing of ideas that are new but false or unimportant, or true and important, but already well studied under a different branding.

It has been argued here that the discontent is better understood as stemming from a few inescapable properties of living things, which lead to disappointment with evolutionary biology, and a nagging feeling that reform must be overdue.

Evolutionary biology, like history, but unlike other natural sciences, raises issues of purpose and agency, alongside those of complexity and generality

https://link.springer.com/article/10.1007/s10539-016-9557-8?fbclid=IwAR37cKt9BHLC8m4W2YCxYLR9ywLp9Z3-WxSVKm0lPmkEguDYm6MAZvYvTFw

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A duplication mutation that doesn't add any de novo, 3-D, coded meta information to the genome and so is utterly irrelevant to any macroevolutionary discussion. Learn the subject will ya? Random drift of neutral mutations and duplication of preexisting information along with purifying selection eliminating deleterious mutations is the recognized mode for neo-Darwnian/modern synthetic evolution which cannot accumulate into macroevolution which requires the constant, consistent addition of de novo 3-D, coded metainformation to multiple protein genes producing de novo functionality which has never been observed.

"Horizontal gene transfer in eukaryotes: The weak-link model"55

Jinling Huang.

Bioessays,.2013 Oct; 35(10): 868–875.

"Given the fact that point mutation, recombination, gene duplication, and genome rearrangement only operate on pre-existing genes..."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033532

“Darwinian evolution in the light of genomics”

Eugene V. Koonin*

Nucleic Acids Res. 2009 Mar; 37(4): 1011–1034.

“Evolutionary-genomic studies show that natural selection is only one of the forces that shape genome evolution and is not quantitatively dominant, whereas non-adaptive processes are much more prominent than previously suspected. Major contributions of horizontal gene transfer and diverse selfish genetic elements to genome evolution undermine the Tree of Life concept. An adequate depiction of evolution requires the more complex concept of a network or ‘forest’ of life. There is no consistent tendency of evolution towards increased genomic complexity, and when complexity increases, this appears to be a non-adaptive consequence of evolution under weak purifying selection rather than an adaptation.
...
The neutral theory and purifying selection

Arguably, the most important conceptual breakthrough in evolutionary biology after the Modern Synthesis was the neutral theory of molecular evolution that is usually associated with the name of Kimura...According to the neutral theory, a substantial majority of the mutations that are fixed in the course of evolution are selectively neutral so that fixation occurs via random drift...What the theory actually maintains is that the dominant mode of selection is not the Darwinian positive selection of adaptive mutations, but stabilizing, or purifying selection that eliminates deleterious mutations while allowing fixation of neutral mutations by drift....

With regard to the contribution of duplication to the origin of new genes, it is important to note that there is little compelling evidence of de novo emergence of genes from non-coding sequences...Hence it is tempting to generalize that gene duplication is not just an important but indeed the dominant route that leads to the origin of new genes...an evolutionary mode that obliterates detectable connections to the original source"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2651812/...

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Physical foundations of biological complexity

The apparent abrupt surges of complexity during evolution are embodied in the concept of major and minor evolutionary transitions and, under a different perspective, in the concept of punctuated equilibrium. From a physical standpoint, a rise in complexity is linked to the widespread phenomenon of self-organized criticality (SOC). SOC is a property of dynamical systems with extended degrees of freedom and pronounced nonlinearity whereby the system goes through serial “avalanches” separated in time by intervals of stability. Under the original SOC concept, self-similar (power-law) scaling of avalanche sizes is the distinctive feature of the critical dynamics. Here, however, we adopt a more general view of SOC whereby the largest avalanches that appear in the characteristic lifetime of the system are on the scale commensurate with the system size.

The behavior of systems with SOC dynamics is obviously reminiscent of the punctuated equilibrium model in evolutionary biology, which involves pronounced temporal discontinuities in evolutionary innovation. This analogy has not escaped the attention of the architects of the SOC concept, who constructed models directly inspired by biological systems and intended to mimic their behavior.

My comment. It is remarkable, what mental gymnastics the authors must make in order to press the evidence into a framework where naturalism & evolution fits. `The apparent abrupt surges of complexity during evolution` is begging the question, where evolution is like putting the Cart before the horse. That's bad science. That's a hopeless attempt to fix what is broken. To do so, new, smart-sounding names are invented. Self-organized criticality (SOC).
Another way of begging the question.

https://www.pnas.org/content/115/37/E8678

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https://www.youtube.com/watch?v=hOfRN0KihOU&feature=youtu.be&fbclid=IwAR3Igus_XPbr35V5_EH-PQuRO3puKKw-f4ET5f-oXshDM1D_T2V7ZwG_ruY



Claim: chromosomes hold the DNA DNA consists of different genes and it's these genes that are life's information carriers they contain instructions and orders for the cells and determine the characteristics and traits that living creatures have.
Response:  Genetic AND epigenetic factors define body-form, architecture, phenotype and species. 

Six determining factors are genetic: 

1. Homeobox and Hox genes determine the shape of the body.
2. Noncoding DNA  ( Junk DNA ) is transcribed into functional non-coding RNA molecules and switches protein-coding genes on or off.
3. Transposons and Retrotransposons regulate genes
4. Centrosomeplay a central role in development
5. The precise arrangement of Cytoskeletal arrays provides critical structural information.
6. Egg-polarity genes encode macromolecules deposited in the egg to organize the axes

And following nine mechanisms, amongst it, 23 epigenetic codes and languages, are ultimately not sourced back to genes, but several epigenetic mechanisms. 

1. The Gene regulation network orchestrates gene expression
2. Various signalling pathways generate Cell types and patterns
3. At least 23 Epigenetic Codes are multidimensional and perform various tasks essential to cell structure and development
4. Cell-Cell communication in various forms, especially important for animal development
5. Chromatin dance in the nucleus through extensile motors affect transcription and gene regulation
6. Post-transcriptional modifications (PTMs) of histones affect gene transcription
7. The DNA methylation code is like a barcode or marker, the methyl group indicates, for instance, which genes in the DNA are to be turned on.
8. Membrane targets provide crucial information—spatial coordinates—for embryological development.
9. Ion Channels and Electromagnetic Fields influence the form of a developing organism
10. The Sugar Code forms information-rich structures which influence the arrangement of different cell types during embryological development.
11. Hormones  are special chemical messengers for development

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-Mutation - the vast majority are negative.
Toward a realistic model of mutations affecting fitness. Keightley & Lynch, 2003, Evolution, 57:683 {685, 2003) https://onlinelibrary.wiley.com/.../j.0014-3820.2003... "...THE VAST MAJORITY OF MUTATIONS ARE DELETERIOUS. THIS IS ONE OF THE MOST WELL-ESTABLISHED PRINCIPLES OF EVOLUTIONARY GENETICS, SUPPORTED BY BOTH MOLECULAR AND QUANTITATIVE-GENETIC DATA."
"...a great deal of evidence from several sources strongly suggests that the overall effects of mutations are to REDUCE FITNESS."

"All of these experiments detected DOWNWARD trends in MA (mutation accumulation) line population mean fitness relative to control populations as generations accrued. As far as we know, there is NO CASE of even a single MA line maintained by bottle-necking that showed significantly higher fitness than its contemporary control populations."
"Ethyl methanesulfonate (EMS) mutagenesis experiments, in which controls are given identical treatment to mutagenized lines, other than a dose of mutagen, have also shown consistently strongly NEGATIVE EFFECTS on fitness traits in Drosophila."

"Similarly, transposable element insertional mutagenesis leads to REDUCED fitness in Drosophila."
"Although the above studies have focused on the fitness effects of mutations in the context of laboratory environments, substantial indirect evidence derived from molecular studies supports the contention that MOST MUTATIONS IN NATURAL POPULATIONS ARE DELETERIOUS."

"If mutations are neutral on average, C, the proportion of ‘missing’ amino-acid substitutions, would have an expected value of 0.0. However, IN ALL TAXA EXAMINED SO FAR, average values of C are in excess of 0.7, implying that the MAJORITY of amino-acid altering mutations are deleterious."

"The 214 generation experiment of Vassilieva et al. (2000) clarifies the slowly emerging pattern — as the period of MA (mutation accumulation) extended, PROGRESSIVELY LOWER FITNESS CLASSES ACCUMULATED, whereas the frequencies of the highest fitness classes observed in the controls PROGRESSIVELY DIMINISHED. Contrary to the suggestions of Shaw et al. (2002), there is NO EVIDENCE for improved fitness IN ANY periodically bottlenecked C. elegans line." (all emphasis added)

-Selection - has absolutely no ability to generate anything in order to add complexity... it's nothing more than what is already available.
-Sexual intercourse - actually constrains major change...

From the article below...
Heng and fellow researcher Root Gorelick, Ph.D., associate professor at Carleton University in Canada, propose that although diversity may result from a combination of genes, the primary function of sex is NOT about promoting diversity. Rather, it’s about keeping the genome context — an organism’s complete collection of genes arranged by chromosome composition and topology — as UNCHANGED as possible, thereby maintaining a species’ identity. This surprising analysis has been published as a cover article in a recent issue of the journal Evolution.

“If sex was merely for increasing genetic diversity, it would NOT have evolved in the first place,” said Heng. This is because asexual reproduction — in which only one parent is needed to procreate — leads to HIGHER rates of genetic diversity than sex.
In fact, two billion years ago in Earth’s biosphere, life relied exclusively on asexual reproduction, and every organism was capable of bearing young without costly competition to mate. With asexual species’ faster and more efficient mode of reproduction, the origin and maintenance of sex — not exactly the fittest means of reproduction — puzzles scientists, who for decades have been asking, Why has sex evolved and survived?
According to Heng, the hidden advantage sex has over asexual reproduction is that it CONSTRAINS MACROEVOLUTION — evolution at the genome level — to allow a species’ identity to survive. In other words, it PREVENTS “Species A” from morphing into “Species B.” Meanwhile, it also allows for microevolution — evolution at the gene level — to allow members of the species to adapt to the environment.
https://www.sciencedaily.com/rel.../2011/07/110707161037.htm

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What’s wrong with evolutionary biology?
https://link.springer.com/article/10.1007/s10539-016-9557-8

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Rui Diogo Quasi-religious Belief in Darwin and Darwinism: “Straw-Men” Scientist Believers Everywhere 2 June 2020

Narratives that describe models of how the world works involve some form of idealization, but all models are subjective and influenced by many human factors including the location, period of time, and profession of the narrator. Charles Darwin is a particularly fascinating case. Many scientists have tended—and continue—to idealize him as a person and a scientist, as well as his evolutionary ideas, in particular those related to “adaptationism” and the “struggle for existence.” In fact, many still defend that there is no need for any kind of new or even “extended” evolutionary theories: what we have from Darwin, or from the subsequent “Modern Synthesis,” is enough, as if the thousands of studies made in the last decades, including the discovery of the DNA, the genomes of humans and other species, or the crucial evolutionary role played by epigenetics, did not add anything relevant to how we understand biological evolution. Interestingly, such reactions are somehow comparable with those of some religious leaders that, when certain scientific discoveries contradict narratives of a religious text, argue that these are just “minor” details that do not put those narratives into question. An example concerns certain adaptationist narratives, which as Gould noted cannot be falsified: by assuming a priori that a structure has to have an “adaptive function,” even when hypotheses that the function is A, B, C, or D are contradicted, one tries to show that perhaps the function is E, or F, and so on, instead of being at least open to the hypothesis that perhaps those “negative results” mean that the structure has no current “adaptive function.” Such circular reasoning is deeply related to another common feature of humans-the-storytelling-animals: our continuous search for “purpose.” As the founder of biology, Aristotle, famously stated, nature “does nothing in vain”—a teleological notion that deeply influenced Darwin, and continues to influence us. The aim of this paper is not to criticize Darwin—I profoundly admire his life, travels, persistence, naturalism, and brilliant ideas such as that of natural selection. Instead, here, I discuss subjects such as adaptationism and the notions of progress, purpose, and “struggle for life” and their links to racism and misogyny to call attention to the remarkable parallel between religious thinking and the inflexible way in which many defend Darwin’s, Darwinist, or NeoDarwinist ideas, even when such ideas might have contributed to enduring biases and prejudices within both the scientific community and broader society.


“like the hand of Providence in the biblical account, natural selection justifies even where it fails to explain … what happens is not always ‘right’ or well understood, but it is ‘fit’.”


Conclusions 
1. Charles Darwin provides a very clear illustration of how strong is our human tendency to idealize—so many scientists continue to venerate him as a person or to defend all his evolutionary ideas or even the more extreme “adaptationist,” struggle for existence versions later postulated by several so-called “Neo-Darwinists.” 
2. A main problem with Darwin and many of his subsequent followers is that those parts of their works used by adaptationists, racists, white supremacists and misogynists to support their ideas are neither “good ideas” nor scientifically correct. 
3. The main here aim is not to criticize Darwin, but to call attention to the remarkable parallel between religious thinking and the inflexible—sometimes unfalsifiable— way in which many defend Darwin’s or Neo-Darwinist ideas, even in such cases when they are plain wrong. 
4. For creationists that would use this paper to criticize evolutionists in general, I should note that I am above all criticizing the quasi-religious reasoning done by many scholars, so it would be a paradox—and also plain wrong—to use this criticism to defend the type of religious thinking of creationists. Actually, the fact that I, an evolutionist, am criticizing the quasi-religious

1. https://sci-hub.ren/10.1007/s40610-020-00127-y

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Hiroshi Akashi: Molecular Evolution in the Drosophila melanogaster Species Subgroup: Frequent Parameter Fluctuations on the Timescale of Molecular Divergence 2006 Mar 4
Although mutation, genetic drift, and natural selection are well established as determinants of genome evolution, the importance (frequency and magnitude) of parameter fluctuations in molecular evolution is less understood. The magnitude, timescale, and genomic breadth of fluctuations in molecular evolutionary forces remain to be studied systematically. Such knowledge is critical for modeling the causes of molecular evolution and is necessary for designing tests of adaptive and deleterious evolution and methods for phylogenetic inference and ancestral state reconstruction.

My comment: An important admission: In order to claim that primary speciation is true ( phyletic speciation, that is the transformation of one species into another one. ), one would have to know the importance of these frequencies and magnitude, amongst many other things. 



Anna Maria Langmüller: Low concordance of short-term and long-term selection responses in experimental Drosophila populations  February 06, 2020 1

Introduction
Only a subset of the selection targets are detected at earlier generations, which are not representative of the underlying adaptive architecture.

Selection signatures detected early in the experiment are not representative of the underlying adaptive architecture
This study focused on the comparison of selection targets detected at early and late time points. Since analyses based on single SNPs a are very stochastic, we investigated the fraction of candidate SNPs comprising a haplotype block that were also discovered at earlier time points (HADR). We detected 10 haplotype blocks with elevated HADR in generation 20. We found that EDHAs do not differ in their starting allele frequency, haplotype block length, average recombination rate or absolute selection coefficients from other haplotype blocks. EDHAs are, however, more strongly selected at the beginning of the experiment, but are equally strongly selected as the remaining haplotype blocks at later generations. Consistent with stronger selection at earlier time points, the selection signature of EDHAs is significantly more parallel across replicates after 20 generations of adaptation in both empirical and simulated data.. We attribute this observation to a phenomenon similar to the “winners curse”, that is that loci where stochastic effects increased the frequency in multiple replicates to enhance the contribution by selection are more likely to be detected.

All statistical tests, which are evaluating a parallel selection signature across replicates, are more likely to detect selection signatures shared across replicates, even with only moderate allele frequency changes. This could result in a biased picture of the underlying genetic architecture. The analysis of selection signatures in replicated experiments running for only a moderate number of generations is more likely to detect parallel than replicate specific selection signatures. This bias is not restricted to our study, but also an experimental study of D. simulans populations adapting 10 to 20 generations to a new temperature regime (Kelly and Hughes (2018)) found more parallel selection responses. We propose that additional analyses contrasting selection signatures of early and late time points are needed to confirm the enrichment of parallel selection signatures in short-term experiments.

My comment: So even last year, in 2020, there was no scientific confirmation of enrichment of parallel selection signatures in short-term experiments.

JM Akey:Parallel Selection: Evolution’s Surprising Predictability 2012  2
Understanding the molecular and mechanistic basis of adaptation remains a fundamental goal of evolutionary biology.

My comment: Admitting that science in 2012 has not yet a full answer on that question is a remarkable admittance. Nonetheless, proponents of evolution are absolutely confident that such an answer is already at their disposition, and that the traditionally proposed evolutionary mechanisms provide it. But is that really so?

Daniel L. Rabosky:  Effects of evolutionary history on genome wide and phenotypic convergence in Drosophila populations (2018)
Results
We find that, with the exception of longevity and to a lesser extent fecundity, 230 generations of relaxed selection has erased the extreme phenotypic differentiation previously found. We also find no signs of genetic fixation, and only limited evidence of genetic differentiation between previously desiccation resistance selected populations and their controls.

My comment: Rather than providing increased differentiation, the result of the experiments have shown the CONTRARY!!

a: Single nucleotide polymorphisms (SNPs) are a type of polymorphism involving variation of a single base pair. Scientists are studying how single nucleotide polymorphisms, or SNPs (pronounced "snips"), in the human genome correlate with disease, drug response, and other phenotypes.

1. https://www.biorxiv.org/content/10.1101/759704v2.full
2. https://www.cell.com/current-biology/pdf/S0960-9822(12)00406-X.pdf
3. https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-018-5118-7
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456288/

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Ryohei Seki Functional roles of Aves class-specific cis-regulatory elements on macroevolution of bird-specific features 06 February 2017 1

It has been argued for several decades that the phenotypic variations within and between species can be established by modification of cis-regulatory elements, which can alter the tempo and mode of gene expression1. Nevertheless, we still have little knowledge about the genetic basis of macroevolutionary transitions that produced the phenotypic novelties that led to the great leap of evolution and adaptation to new environment. Although numerous efforts have been made to study the evolutionary roles of newly evolved genes in a limited numbers of model species2, little is known about how the genetic changes underlying the major transitions occurred in the deep time, and how they were maintained through long-term macroevolution.

1. https://www.nature.com/articles/ncomms14229

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Stochastic genetic mutations in the coding sequences of a gene should confer the allele variations, that natural selection picks from, and fixes in the gene pool of the population if it confers an advantage of survival, and adaptation to the environment. Gene mutations result in codon mutations, and rather than one, another amino acid is translated and incorporated into a protein amino acid chain. Then, that different sequence should/would theoretically either a) not cause any functional change of a protein, b) deteriorate the protein function, or b) improve or confer a new protein or enzyme function.

In order to say that macroevolution through natural selection, genetic drift, or gene flow is what actually promotes biodiversity, science should be able to detect what genetic mutations, and consequently, altered amino acid sequences provoke. Guess what??
Scientists have no clue!!

Proteome-wide identification of amino acid substitutions deleterious for protein function April 09, 2022.

" DNA sequencing has led to the discovery of millions of mutations that change the encoded protein sequences, but the impact of nearly all of these mutations on protein function is unknown. "

Yes. You heard that right !!! If it is unknown how mutated protein sequences impact protein function, it also cannot be known if evolutionary mechanisms are those that provoke new protein functions, and as such, new body plans, new species, and new functions in new organisms !!

Another point: Proteins have a zip code, a tag, which is like a GPS system, directing them to the place of operation. And there is other genetic information, that directs how proteins have to be inserted in, let, say, for example, a cell membrane. If somehow, the genetic mutation would produce a protein with a new function, that new function would maybe be useful at an entirely different place in the cell, then its genitor. That means, there would have to be completely new information to direct the novel protein to another place in the cell, and more new information to insert it where it is operational.

In order to have a new function, for a new working biological system to be built, the five following conditions would all have to be met:

C1: Availability. Among the parts available for recruitment to form the system, there would need to be ones capable of performing the highly specialized tasks of individual parts, even though all of these items serve some other function or no function.
C2: Synchronization. The availability of these parts would have to be synchronized so that at some point, either individually or in combination, they are all available at the same time.
C3: Localization. The selected parts must all be made available at the same ‘construction site,’ perhaps not simultaneously but certainly at the time, they are needed.
C4: Coordination. The parts must be coordinated in just the right way: even if all of the parts of a system are available at the right time, it is clear that the majority of ways of assembling them will be non-functional or irrelevant.
C5: Interface compatibility. The parts must be mutually compatible, that is, ‘well-matched’ and capable of properly ‘interacting’: even if subsystems or parts are put together in the right order, they also need to interface correctly.

( Agents Under Fire: Materialism and the Rationality of Science, pgs. 104-105 (Rowman & Littlefield, 2004). HT: ENV.)

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Most 'silent' genetic mutations are harmful, not neutral, a finding with broad implications
https://phys.org/news/2022-06-silent-genetic-mutations-neutral-broad.html?fbclid=IwAR0q7YAj93-unG5VZAhCP6zP-3uQvKUPHQRByA_vGoiiXScEf0KO0QE2u4I

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Theory of Evolution? Toppling the Idol of "Settled Science"

https://www.breakpoint.org/which-theory-of-evolution-toppling-the-idol-of-settled-science/

In 1973, evolutionary biologist Theodosius Dobzhansky wrote that “nothing in biology makes sense except in light of evolution.” Almost 50 years later, an increasing number of scientists are asking whether evolution makes any sense in light of what we now know from biology.

A recent long-form essay in The Guardian signals just how urgent the problem has become for the most dominant theory in the history of the sciences. In it, author Stephen Buranyi, gives voice to a growing number of scientists who think it’s time for a “new theory of evolution.”

For a long time, descent with slight modifications and natural selection have been “the basic” (and I’d add, unchallengeable) “story of evolution.” Organisms change, and those that survive pass on traits. Though massaged a bit to incorporate the discovery of DNA, the theory of evolution by natural selection has dominated for 150 years, especially in biology. The “drive to survive” is credited as the creative force behind all the artistry and engineering we see in nature.

“The problem,” writes Buranyi, is that “according to a growing number of scientists,” this basic story is “absurdly crude and misleading.” For one thing, Darwinian evolution assumes much of what it needs to explain. For instance, consider the origin of light-sensitive cells that rearranged to become the first eye, or the blood vessels that became the first placenta. How did these things originate? According to one University of Indiana biologist, “we still do not have a good answer. The classic idea of gradual change, one happy accident at a time,” he says, “has so far fallen flat.”

This scientific doubt about Darwin has been simmering for a while. In 2014, an article in the journal Nature, jointly authored by eight scientists from diverse fields, argued that evolutionary theory was in need of a serious rethink. They called their proposed rethink the “Extended Evolutionary Synthesis,” and a year later, the Royal Society in London held a conference to discuss it.

Along with Darwinian blind spots like the origin of the eye, the Extended Synthesis seeks to deal with the discovery of epigenetics, an emerging field that studies the inherited traits not mediated by DNA. Then there are the rapid mutations that evade natural selection, a fossil record that appears to move in “short concentrated bursts” (or “explosions”), and something called “plasticity,” which is the ability we now know living things have to adapt physically to their environments in a single generation without genetically evolving.

All of these discoveries—some recent, others long ignored by mainstream biology—challenge natural selection as the “grand theory” of life. All of them hint that living things are greater marvels and mysteries than we ever imagined. And, unsurprisingly, all of these discoveries have been controversial.

The Guardian article described how Royal Society scientists and Nobel laureates alike boycotted the conference, attacking the extended synthesis as “irritating” and “disgraceful,” and its proponents as “revolutionaries.” As Gerd Müller, head of the department of theoretical biology at the University of Vienna helpfully explained, “Parts of the modern synthesis are deeply ingrained in the whole scientific community, in funding networks, positions, professorships. It’s a whole industry.”

Such resistance isn’t too surprising for anyone who’s been paying attention. Any challenges to the established theory of life’s origins, whether from Bible-believing scientists or intelligent design theorists, have long been dismissed as religion in a lab coat.

The habit of fixing upon a dogma and calling it “settled science” is just bad science that stunts our understanding of the world. It is a kind of idolatry that places “science” in the seat of God, appoints certain scientists as priests capable of giving answers no fallible human can offer, and feigns certainty where real questions remain. The great irony is that this image of scientist-as-infallible-priest makes them seem like the caricature of medieval monks charging their hero Galileo with heresy for his dissent from the consensus.

As challenges to Darwin mount, we should be able to articulate why “settled science” makes such a poor god. And we should encourage the science and the scientists challenging this old theory-turned-dogma, and holding it to its own standards. After all, if Darwinian evolution is as unfit as it now seems, it shouldn’t survive.

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Frank Zindler, President of American Atheists,  in 1996
The most devastating thing though that biology did to Christianity was the discovery of biological evolution. Now that we know that Adam and Eve never were real people the central myth of Christianity is destroyed. If there never was an Adam and Eve there never was an original sin. If there never was an original sin there is no need of salvation. If there is no need of salvation there is no need of a Savior. And I submit that puts Jesus, historical or otherwise, into the ranks of the unemployed. I think that evolution is absolutely the death knell of Christianity.

Reply: The two basic tenets upon which the theory of evolution rests, are the claim of universal common ancestry, and the tree of life. The two claims have been refuted on many grounds. When we talking about the tree of life, we cannot overlook the origin of viruses. Eugene V. Koonin admitted openly in 2020: In the genetic space of viruses and MGEs, no genes are universal or even conserved in the majority of viruses. Viruses have several distinct points of origin, so there has never been a last common ancestor of all viruses. The universal common ancestry of life is also disputed. For example  Eric Bapteste, evolutionary biologist: "We have no evidence at all that the tree of life is a reality." DAVID M. RAUP, paleontologist: Multiple origins of life in the early Precambrian is a reasonable possibility. And C.P. Kempes in the peer-reviewed article: The Multiple Paths to Multiple Life (2021): We argue for multiple forms of life realized through multiple different historical pathways. In regard to the origin of humans: All human beings are 99.9 percent identical in their genetic makeup. Harmful protein-coding mutations in people arose largely in the past 5,000 to 10,000 years. Evidence for a Human Y Chromosome Molecular Clock: Pedigree-Based Mutation Rates Suggest a 4,500-Year History for Human Paternal Inheritance. By comparing the mitochondrial DNA of 147 people from five different ethnic groups, the researchers found that all the individuals analyzed were descendants of the same female lineage, that is, they all had the same original "mother" at the beginning of everything. Thus, they confirmed that all humanity descends from the same woman, who would have been the first Homo sapiens. And they called her "Mitochondrial Eve". These few quotes demonstrate that the major evolutionary tenets are far from being a scientific fact, or consensus among specialists in the field. Adding the complete failure of abiogenesis research permits the inference from eliminative induction:

The most devastating thing though that biology has done to naturalism is the failed claim of chemical and biological evolution. Now that we know that Adam and Eve were real people the central creation narrative of Christianity is confirmed. If there was an Adam and Eve there was an original sin. If there was an original sin there is need of salvation. If there is need of salvation there is need of a Savior. And I submit that puts Jesus, historical or otherwise, into the ranks of the necessary. I think that the failure of abiogenesis and evolution is absolutely the death knell of naturalism.

Common descent, the tree of life, a failed hypothesis
https://reasonandscience.catsboard.com/t2239-evolution-common-descent-the-tree-of-life-a-failed-hypothesis

Human origins: Created, or evolved?
https://reasonandscience.catsboard.com/t2683-is-the-genesis-account-of-literal-6-days-just-a-myth#8168

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C. S. Roberts (2012): The three limitations of Darwin's theory concern the origin of DNA, the irreducible complexity of the cell, and the paucity of transitional species. Because of these limitations, the author predicts a paradigm shift away from evolution to an alternative explanation. The intellectual problem is that it remains a suspect theory >150 years after the publication of The Origin of Species (1859). 
https://www.tandfonline.com/doi/abs/10.1080/08998280.2012.11928782

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Why evolution fails

Suppose we have a factory that produces calculators, and we want to examine whether it is possible for the factory to evolve into a computer factory through gradual changes. In this scenario, manufacturing errors occasionally introduce variations in the calculators. If one of these variations happens to improve the calculator's functionality, it gains popularity among users, and the factory incorporates the change permanently. However, the transition from a calculator factory to a computer factory presents substantial challenges. A calculator is a relatively simple device that performs basic arithmetic operations and has a limited number of buttons for numerical input. On the other hand, a computer requires complex processing capabilities, storage, input/output devices, an operating system, and various software applications. Suppose a manufacturing error occurs, resulting in a calculator with slightly more memory or a larger display. While these changes may enhance the calculator's functionality, they would not be sufficient for it to become a computer. Additional components such as a keyboard, storage units, a monitor, and interfaces for peripherals would be required. However, these components cannot be easily modified or duplicated from existing calculator parts. Even if, by chance, a neighboring factory accidentally supplies a computer's motherboard to the calculator factory, numerous specific modifications would still be necessary to integrate it with the existing calculator components. The calculator's buttons would need to be reconfigured as keys, the display would have to be upgraded to a monitor, and various new interfaces and connections would need to be developed from scratch. The transition from a calculator to a computer also involves significant changes in the manufacturing processes and production flow. Computer manufacturing requires advanced techniques such as printed circuit board assembly, soldering, and chip integration, which differ substantially from the processes used in calculator production. The factory would need to acquire new machinery, retrain its workforce, and establish new quality control measures specific to computer production. Moreover, the transition would require the introduction of entirely different raw materials and supply chains. Computer components like integrated circuits, processors, memory modules, and hard drives would need to be sourced and integrated into the production process. This would require establishing relationships with new suppliers, implementing specialized import mechanisms, and incorporating additional testing and validation procedures. Additionally, the factory would need to adapt its production lines and infrastructure to accommodate the assembly of computers. The manufacturing process would become more complex, involving the installation of different components, the integration of software systems, and the testing and quality assurance of the final product. The transition from a calculator factory to a computer factory involves far more than just gradual modifications or adaptations. It requires the integration of specialized components, the development of complex interactions and systems, the acquisition of new machinery, the implementation of advanced manufacturing techniques, the sourcing of different raw materials, and the establishment of new supply chains and quality control measures. While biological evolution through gradual accumulation of unguided errors is a valid concept, applying it directly to the complex transition from a calculator to a computer poses significant challenges that go beyond simple modifications and adaptations within the existing production process.


Let me give you a real-life example:

AIR carboxylase catalyzes the carboxylation of aminoimidazole ribotide (AIR) using bicarbonate (HCO−3/CO2) as the source of the carboxyl group.  Carboxylation refers to the addition of a carboxyl group (-COOH) to a molecule. In the context of biochemical reactions, carboxylation typically involves the addition of a carbon dioxide molecule (CO2) to a substrate, resulting in the formation of a carboxyl group. Carboxylation reactions are common in various metabolic pathways and have important roles in the synthesis of many essential biomolecules. The addition of a carboxyl group can introduce new chemical functionalities, alter the charge or polarity of a molecule, or create binding sites for other molecules or enzymes.

The enzyme AIR carboxylase catalyzes the carboxylation of aminoimidazole ribotide (AIR) using bicarbonate (HCO−3/CO2) as the source of the carboxyl group. This carboxylation reaction leads to the formation of carboxyaminoimidazole ribotide (CAIR), which serves as an intermediate in the synthesis of purine nucleotides.  The carboxylation reaction catalyzed by PurE alone in the purine biosynthesis pathway has a relatively high KM value for bicarbonate (HCO−3), which means that it has a low affinity for the substrate. The KM value represents the concentration of substrate at which the enzyme operates at half of its maximum velocity. KM, or the Michaelis-Menten constant, is a parameter used to describe the affinity of an enzyme for its substrate. It is named after Leonor Michaelis and Maud Menten, who developed the Michaelis-Menten equation to describe enzyme kinetics. The KM value represents the substrate concentration at which an enzyme operates at half of its maximum velocity (Vmax). In other words, it quantifies the concentration of substrate required for an enzyme to achieve half of its catalytic efficiency. Enzymes with a low KM value have a high affinity for their substrate, meaning they can effectively bind and catalyze the reaction even at low substrate concentrations. On the other hand, enzymes with a high KM value have a lower affinity for their substrate and require higher substrate concentrations to achieve the same catalytic efficiency. The KM value is influenced by several factors, including the strength of the enzyme-substrate interaction, the stability of the enzyme-substrate complex, and the rate at which the enzyme converts the substrate into a product. In the context of the carboxylation reaction catalyzed by PurE, the relatively high KM value for bicarbonate indicates that PurE has a lower affinity for bicarbonate. It means that PurE requires a higher concentration of bicarbonate to efficiently catalyze the carboxylation reaction compared to an enzyme with a lower KM value.

In the case of PurE, its high KM value for bicarbonate indicates that it requires a relatively high concentration of bicarbonate to effectively catalyze the carboxylation reaction. The reported KM value of approximately 110 mM suggests that the enzyme would need bicarbonate concentrations around 100 mM to proceed at a reasonable rate. In biochemistry, mM stands for millimolar, which is a unit of concentration. It represents the number of millimoles of a substance per liter of solution. A mole (mol) is a unit used to measure the amount of a substance, and millimole (mmol) is one-thousandth of a mole. Concentrations expressed in millimolar (mM) are commonly used to describe the concentration of solutes in biological systems.  Such a high bicarbonate concentration is considered unphysiological because the intracellular concentration of bicarbonate in cells is typically much lower, ranging from a few millimolar to tens of millimolar. Therefore, if PurE were the sole enzyme responsible for the carboxylation reaction, it would require an excessive amount of bicarbonate that is not typically present in the cellular environment. To overcome this limitation and ensure efficient carboxylation, the purine biosynthesis pathway in organisms like yeast, plants, and most prokaryotes, including E. coli, utilizes a two-protein system consisting of PurE and PurK. PurK acts as a helper protein and interacts with PurE to enhance the efficiency of the carboxylation reaction.

If the helper protein PurK is not present in the purine biosynthesis pathway, and only the enzyme PurE is active, it would have several consequences: PurE alone would still be able to catalyze the carboxylation reaction, but with a lower efficiency. This is because PurK enhances the efficiency of the reaction by reducing the concentration of bicarbonate (HCO−3) required for PurE to function optimally. PurK acts as a helper protein and interacts with PurE to enhance the efficiency of the carboxylation reaction. It reduces the required concentration of bicarbonate by more than 1000-fold, making the reaction more feasible under physiological conditions. Without PurK, PurE would have a higher KM value for bicarbonate, meaning it would require a higher concentration of bicarbonate to achieve the same catalytic efficiency.  This higher bicarbonate requirement would be unphysiological, as it would exceed the typical bicarbonate concentrations found in cells.  Bicarbonate can be produced as a byproduct of various metabolic reactions within the cell. For example, during the breakdown of certain molecules, such as amino acids or carbohydrates, bicarbonate can be generated as part of the metabolic pathway. Consequently, the pathway might be less efficient in converting substrates to products.  The absence of PurK could potentially disrupt the metabolic flux through the purine biosynthesis pathway. The decreased efficiency and higher bicarbonate requirement of PurE alone may lead to a reduction in the production of downstream intermediates and final purine products. This could result in a decreased availability of purines for essential cellular processes such as DNA and RNA synthesis.

There are organisms that have alternative pathways for purine biosynthesis that do not require the helper protein PurK. One example is the archaeon Methanocaldococcus jannaschii, which lacks the PurK protein but still synthesizes purines. The absence of PurK in certain organisms can be attributed to adaptations and the development of alternative enzymatic reactions. These organisms have different mechanisms to achieve the same end result, which is the production of purines. In the case of Methanocaldococcus jannaschii, it has been found that it utilizes a distinct enzyme, known as PurP, to catalyze the carboxylation reaction instead of relying on PurK. PurP is capable of directly carboxylating the purine precursor in a manner that is independent of ATP hydrolysis. The presence or absence of PurK in different organisms likely reflects diversification and adaptation to specific environmental conditions. Organisms lacking PurK may have acquired alternative pathways to optimize their purine biosynthesis based on their unique ecological niches or metabolic requirements.

Methanocaldococcus jannaschii using PurP, and an entirely different enzyme for the same biosynthesis step in purine synthesis

Methanocaldococcus jannaschii, a methanogenic archaeon, uses PurP instead of the traditional PurE and PurK enzymes found in other organisms. The specific reason for this adaptation in Methanocaldococcus jannaschii is related to its unique ecological niche and metabolic requirements. Methanogens are microorganisms that produce methane as a byproduct of their metabolism. They thrive in anaerobic environments, such as deep-sea hydrothermal vents, where they utilize carbon dioxide (CO2) and hydrogen (H2) to produce methane (CH4). This unique metabolic pathway requires efficient utilization of CO2 as a carbon source. PurP, found in Methanocaldococcus jannaschii, has a distinct ability to use CO2 and formate as substrates for the carboxylation step in purine synthesis. This adaptation may be advantageous for Methanocaldococcus jannaschii in environments where CO2 is more abundant or as a means to efficiently incorporate CO2 into essential cellular components, such as purine nucleotides.

Despite catalyzing the same step in purine synthesis, PurP is indeed an entirely different enzyme compared to PurE and PurK. While PurE and PurK are structurally and functionally related enzymes that act as a two-protein system, PurP has and exhibits distinct characteristics. PurP has a different protein structure. It possesses unique catalytic properties, such as utilizing CO2 and formate as substrates instead of bicarbonate. Therefore, while PurP and PurE/K catalyze the same step in purine synthesis, PurP can be considered an enzyme that has emerged independently to fulfill a similar function in different organisms, with structural and functional differences that reflect its unique trajectory of origins. PurP, PurE, and PurK have distinct structural and functional characteristics that allow them to be distinguished from one another.

PurP has a distinct protein structure compared to PurE and PurK. The amino acid sequence and overall folding of PurP are different, resulting in a unique three-dimensional architecture. While PurE and PurK primarily use bicarbonate as a substrate, PurP has a broader substrate specificity. PurP can utilize CO2 and formate as substrates for the carboxylation reaction, distinguishing it from PurE and PurK. The catalytic mechanisms of PurP, PurE, and PurK may differ due to their structural variations and specific active site configurations. These differences may affect how they interact with substrates and carry out the carboxylation reaction. PurP, PurE, and PurK exhibit different levels of catalytic efficiency. Each enzyme has unique kinetic properties, such as turnover rate (kcat) and substrate affinity (KM), which influence their overall efficiency in the purine synthesis pathway.  The genes encoding PurP, PurE, and PurK may have distinct DNA sequences and regulatory elements. Differences in gene expression patterns, transcriptional regulation, and protein synthesis contribute to the differential production and presence of these enzymes in different organisms.  PurP, PurE, and PurK likely have different origins. While PurE and PurK are structurally and functionally related enzymes that form a two-protein system, PurP represents a distinct enzyme that has emerged independently in certain organisms.

The distinct protein structures and catalytic properties of PurP, PurE, and PurK provide compelling evidence that these enzymes were separately designed for their specific functions in different organisms. The remarkable complexity and specificity of these enzymes make it highly unlikely that they could have arisen through a gradual step-by-step evolutionary process. The unique features exhibited by PurP, PurE, and PurK are finely tuned to perform their specific roles in purine synthesis. Any significant changes in their amino acid sequences or protein structures would likely disrupt their functionality, rendering them ineffective or even non-functional. To transition from one species to another, these enzymes would require substantial modifications. However, the probability of random mutations producing the precise sequence and structural changes necessary for functional enzymes in different organisms is astronomically low. The intricate interplay between the amino acid residues and the overall three-dimensional structure of these enzymes is finely balanced and optimized for their respective catalytic activities. Such complex, finely-tuned design and functionality could only be the result of deliberate and purposeful design by an intelligent agent. These enzymes serve their specific functions in different organisms, rather than emerging through an undirected, gradual process of evolution.

Premise 1: Proteins with distinct protein structures, catalytic properties, and functional characteristics require specific amino acid sequences and precise three-dimensional configurations to perform their intended functions effectively.
Premise 2: PurP, PurE, and PurK exhibit distinct protein structures, catalytic properties, and functional characteristics.
Conclusion: Therefore, it is highly improbable for PurP, PurE, and PurK to have a common ancestor because the likelihood of random mutations producing the necessary sequence and structural changes to generate these distinct proteins with their specific functionalities is extremely low.


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