We also know very little about gene evolution among gene families and how a gene actually forms another gene putatively by divergence after duplication 2
The kind of papers which are supposed not to exist -- have increasingly been slipping through the net and finding their way into the peer-reviewed literature. One such paper, "Is gene duplication a viable explanation for the origination of biological information and complexity?," authored by Joseph Esfandier Hannon Bozorgmeh and published online last week in the journal, Complexity, challenges the standard gene duplication/divergence model regarding the origin of evolutionary novelty. 1
Is gene duplication a viable explanation for the origination of biological information and complexity?
although the process of gene duplication and subsequent random mutation has certainly contributed to the size and diversity of the genome, it is alone insufficient in explaining the origination of the highly complex information pertinent to the essential functioning of living organisms.
Biologic Institute's Groundbreaking Peer-Reviewed Science Has Now Demonstrated the Implausibility of Evolving New Proteins
In 2011, Ann Gauger and Douglas Axe published a paper in BIO-Complexity, "The Evolutionary Accessibility of New Enzymes Functions: A Case Study from the Biotin Pathway." They reported results of their laboratory experiments trying to convert one enzyme (Kbl2) to perform the function of a very similar enzyme (BioF2), thought to be very closely related to Kbl2. Because these proteins are both members of the GABA-aminotransferase-like (GAT) family, and are believed to be very closely related, this is the sort of evolutionary conversion that evolutionists say ought to be easily accomplished under the standard co-option model. However, after trying multiple combinations of different mutations, they found otherwise:
We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions.
2010 paper by Axe
Evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth. Considering that Kbl2 and BioF2 are judged to be close homologs by the usual similarity measures, this result and others like it challenge the conventional practice of inferring from similarity alone that transitions to new functions occurred by Darwinian evolution.
Now in their new study, "Enzyme Families-Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase [GAT] Family," Reeves, Gauger, and Axe examine nine other enzymes from the same GAT family. Once again, the idea was to see if it is possible to convert them to perform the function of BioF2. They tested proteins that are closer to BioF2, or more distant from BioF2, than the enzyme they tested in their prior study (Kbl2). But all of the proteins studied are in the same family, and are thought to be closely related.
First, they sought to determine if the enzymes could be converted to perform the function of BioF2 through a single mutation. They created mutation libraries with every single possible mutation in those nine enzymes. No BioF2 function was ever detected. As they explain:
The present study has added to our previous examination of these problems in several respects. We have shown, based on sequence alignment of α-oxoamine synthases (a subset of the GAT family), that our previous use of rational design did indeed target regions of Kbl2 that are likely to be functionally significant. Furthermore we have now shown that the lack of a simple evolutionary transition to BioF2 function is not at all unique to our initial choice of Kbl2 as the starting point. Single mutations cannot convert any of eight other members of the GAT family to that function, despite the fact that all of these enzymes are regarded as close evolutionary relatives.
thanks to Philip Cunningham
Naturalism is one huge gap, Naturalism explains nothing! not how the universe came to be, not how life came to be, not how one single gene of protein came to be. In fact, advances in quantum mechanics have shown naturalism to be false.
Gene duplication : They always compare sequences but never give a demonstration ( how it helps in evolution )
Experimental evolution of gene duplicates in a bacterial plasmid model.- 2007
The fate of gene duplicates subjected to diversifying selection was tested experimentally in a bacterial system.,,,
In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow.,,,
This following article will give you a primer on how far off the mark Darwinists are from having any actual empirical support for their 'ahem' theory as to material processes generating functional information:
Hopeless Matzke - David Berlinski & Tyler Hampton (Refutation of all popular examples purporting to show the origination of new information by Darwinian processes) - August 18, 2013
In other experiments led by Gauger and biologist Ralph Seelke of the University of Wisconsin, Superior, their research team broke a gene in the bacterium E. coli required for synthesizing the amino acid tryptophan. When the bacteria's genome was broken in just one place, random mutations were capable of "fixing" the gene. But even when only two mutations were required to restore function, Darwinian evolution got stuck, apparently unable to restore full function.16 This is because it was more advantageous to delete a gene with low functionality or none than it was to continue to express it. This suggests that it is highly unlikely that the standard gene duplication model would produce new complex functions because gene duplicates are likely to be deleted before evolving some new function.
This is the mother of all ad-hoc explanations:
Phylogenetic patterns of emergence of new genes support a model of frequent de novo evolution - 21 February 2013
We suggest that the overall trends of gene emergence are more compatible with a de novo evolution model for orphan genes than a general duplication-divergence model. Hence de novo evolution of genes appears to have occurred continuously throughout evolutionary time and should therefore be considered as a general mechanism for the emergence of new gene functions.
Yup, Orphan genes (comprising 10 to 30% of every new genome sequenced, including humans) can now just ‘poof’ into existence. That whole evolutionary model of functional sequences being selected for in small increments is no good anymore. Need a new gene? Just call on ‘de novo evolution’ to do your dirty work.
Douglas Axe and Ann Gauger Argue that Design Best Explains New Biological Information - Casey Luskin August 26, 2013
Excerpt: Axe and Gauger observe that “The most widely accepted explanation for the origin of new enzymes is gene duplication and recruitment.” However, they cite experimental work showing that a duplicate gene is much more likely to be silenced (because of the costly resources expended in transcribing and translating it) than it is to acquire a new function.
Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model
Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.
Michael Behe finds Loss of Function Mutations Challenge the Darwinian Model - Casey Luskin August 24, 2013
Excerpt: "Because of the many ways in which a gene can be altered to lose function, the LOF mutation would have a rate several orders of magnitude greater than that of the GOF mutation for the duplicated gene."
The regulatory utilization of genetic redundancy through responsive backup circuits - 2006
Excerpt: many such backed-up genes were shown to be transcriptionally responsive to the intactness of their redundant partner and are up-regulated if the latter is mutationally inactivated. … We thus challenge the view that such redundancies are simply leftovers of ancient duplications and suggest they are an additional component to the sophisticated machinery of cellular regulation.
The regulatory utilization of genetic redundancy through responsive backup circuits - 2006
Excerpt: Duplicate genes and paralogous gene families long have been perceived as genomic sources of genetics robustness (1–5). The assumption is that a functional overlap of these genes acts to compensate against mutations. Yet, this very fact also renders redundancy evolutionarily instable (5, 6), and functional overlaps, typically, are rapidly lost because of divergence (7).
Nevertheless, numerous examples of paralogs retaining their functional overlap for extended evolutionary periods (for examples, see refs. 6 and 8–12) suggest that, at least for a fraction of gene pairs, redundancies are conserved throughout evolution despite their predicted instability.,,, In fact, although retention of redundancy is much less frequent than its loss, its widespread existence is nontrivial and cannot (6) be dismissed as leftovers of recent duplication events.,,,
the paradigm that has emerged is that genes that are functionally redundant are not often independently controlled but rather they are regulated by a system that both monitors and responds to their intactness.
Can Random Mutations Create New Complex Features? A Response to TalkOrigins - Casey Luskin June 22, 2012
Excerpt: the (talkorigins) page suggests searching for "gene duplication" on PubMed to find "more than 3000 references" on the topic. These papers, we're meant to assume, show how evolutionary mechanisms can create new information. But a survey of major review articles on gene duplication I published here on ENV in 2010 revealed that the studies never established that mutations could have produced the complex features in question. After taking a close look at this literature, I found:
The NCSE's (and Judge Jones's) citation bluffs have not explained how neo-Darwinian mechanisms produce new functional biological information. Instead, the mechanisms invoked in these papers are vague and hypothetical at best:
*exons may have been "recruited" or "donated" from other genes (and in some cases from an "unknown source");
*there were vague appeals to "extensive refashioning of the genome";
*mutations were said to cause "fortuitous juxtaposition of suitable sequences" in a gene-promoting region that therefore "did not really 'evolve'";
*researchers assumed "radical change in the structure" due to "rapid, adaptive evolution" and claimed that "positive selection has played an important role in the evolution" of the gene, even though the function of the gene was unknown;
*genes were purportedly "cobbled together from DNA of no related function (or no function at all)";
*the "creation" of new exons "from a unique noncoding genomic sequence that fortuitously evolved" was assumed, not demonstrated;
*we were given alternatives that promoter regions arose from a "random genomic sequence that happens to be similar to a promoter sequence," or that the gene arose because it was inserted by pure chance right next to a functional promoter.
*explanations went little further than invoking "the chimeric fusion of two genes" based solely on sequence similarity;
*when no source material is recognizable, we're told that "genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors" because they are simply "hypermutable";
*we even saw "a striking case of convergent evolution" of "near-identical" proteins.
To reiterate, in no case were the odds of these unlikely events taking place actually calculated. Incredibly, natural selection was repeatedly invoked in instances where the investigators did not know the function of the gene being studied and thus could not possibly have identified any functional advantages gained through the mutations being invoked. In the case where multiple mutational steps were involved, no tests were done of the functional viability of the alleged intermediate stages. These papers offer vague stories but not viable, plausibly demonstrated explanations for the origin of new genetic information.
I haven't gone through all "3000 references" cited by TalkOrigins. Neither, in all likelihood, has the author of the TalkOrigins page. But my strong suspicion is that if you went through many of those pages, you'd reach the same conclusion.
This 3000-unnamed-paper citation bluff -- and much other material on this TalkOrigins page, are not to be taken seriously.
Evolution by Gene Duplication Falsified - December 2010
Excerpt: The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. Contrary to Darwin’s view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme—as with RNASE1B in colobine monkeys. The conservation of all-important motifs within gene families, such as the homeobox or the MADS-box motif, attests to the fact that gene duplication results in the copying and preservation of biological information, and not its transformation as something original.
The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway – Ann K. Gauger and Douglas D. Axe – April 2011
Excerpt: We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions. But evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth.
When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
Excerpt: Based on our experimental observations and on calculations we made using a published population model , we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
Gene Duplication and the Origin of Novel Biological Information: A Case Study of the Globins JonathanM - Oct. 2012
Excerpt: In summary, we have seen that the scope for evolution of novel genes and proteins by virtue of gene duplication and subsequent divergence or recruitment is very limited, even in facilitating relatively trivial functional innovations. Given the extremely diverse array of protein conformations found in living systems, the likelihood of the relatedness of genes -- even within gene families -- may be treated with suspicion and healthy skepticism. It is somewhat ironic that biologists are all too willing to accept a statistical argument against two or more proteins with similar sequences arising independently by chance, but are completely unwilling to consider statistical arguments against them arising by chance at all.
Please note in the following study that Darwinists had to first delete a functional gene in order to demonstrate that a preexisting gene could be modified in order to compensate for the deleted gene.,,,
Evolution of New Genes Captured (Oct. 22, 2012)
Excerpt: Nasvall, Lei and Andersson tested this model using the bacterium Salmonella. The bacteria carried a gene involved in making the amino acid histidine that had a secondary, weak ability to contribute to the synthesis of another amino acid, tryptophan. In their study, they removed the main tryptophan-synthesis gene from the bacteria and watched what happened.,,, What emerged was a tryptophan-synthesizing activity provided by a duplicated copy of the original gene.
Mutations and Duplications: Pools of Innovation? - October 23, 2012
Excerpt: The researchers stated that two mutations were required to produce the “innovation” (which was actually more like a “restoration” of a deleted function).
Of course the interesting part in the whole experiment is the part that the Darwinists left out. The part they left out is the fact that the 'evolved' bacteria, with the 'new' tryptophan-synthesizing activity, is in fact less 'fit for survival' than the original bacteria that had the original tryptophan gene knocked out. And thus the burning question remains,,'Where is the evidence that Darwinian evolution can generate functional information over and above that which is already present???'
For a broad outline of the 'Fitness test', required to be passed to show a violation of the principle of Genetic Entropy, please see the following video:
Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video
Michael Behe Hasn't Been Refuted on the Flagellum!
Excerpt: Douglas Axe of the Biologic Institute showed in one recent paper in the journal Bio-complexity that the model of gene duplication and recruitment only works if very few changes are required to acquire novel selectable utility or neo-functionalization. If a duplicated gene is neutral (in terms of its cost to the organism), then the maximum number of mutations that a novel innovation in a bacterial population can require is up to six. If the duplicated gene has a slightly negative fitness cost, the maximum number drops to two or fewer (not inclusive of the duplication itself).
The GS (genetic selection) Principle – David L. Abel – 2009
Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.”
Gene duplication not usually a source of biochemical innovation? - October 2011
Excerpt: Despite a resulting divergence, there remains a distinct preservation of both sequence and functionality among the paralogs. This would indicate that duplicates can be retained by selection for reasons related to their redundant functionality. It also shows that, even when positive selection is inferred in duplicate genes, this may be of a compensatory nature rather than one representing any biochemical innovation.
Gene Duplication and the Origin of Novel Biological Information: A Case Study of the Globins - JonathanM - October 2011
Simulating evolution by gene duplication of protein features that require multiple amino acid residues: Michael J. Behe and David W. Snoke
Excerpt: The fact that very large population sizes—10^9 or greater—are required to build even a minimal [multi-residue] feature requiring two nucleotide alterations within 10^8 generations by the processes described in our model, and that enormous population sizes are required for more complex features or shorter times, seems to indicate that the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular diploid species, because few multicellular species reach the required population sizes.
Genome truncation vs mutational opportunity: can new genes arise via gene duplication?—Part 1 - Royal Truman and Peter Borger
Conclusions: Various evolutionary scenarios were examined by varying parameters such as prokaryote population size, mutational rate, generation times, proportion of population with additional genes, number of duplicate genes and selectivity coefficient favouring genome truncation. Assuming mutations on a duplicate are harmless would permit these to accumulate, but in reality natural selection would systematically remove the descendents of duplication events, drastically limiting both the total number and variety of mutants. Duplicate genes would be created, accumulate at most a very small number of mutations, and then go extinct, again and again. The number of distinct mutational variants generated would be far too small to explain the origin of novel cellular functions. All scenarios using prokaryote populations failed to generate enough mutation to produce novel genes. The most promising approach assumes huge populations would be involved, although subsequently surviving and fixing would now become exceedingly unlikely. Preventing novel gene families from developing denies
nature the necessary infrastructure to produce complex new features. This finding contradicts what is being claimed by evolutionary biologists, which therefore invites other explanations as to the source of genetic complexity to be considered.
A Fishy Story About AntiFreeze Gene Evolution - Casey Luskin - January 2011
Excerpt: In his 2005 textbook Evolution, Douglas Futuyma states that a high estimate of the gene duplication rate is "about 0.01 duplication per gene per million years." (p. 470) A given gene will thus be duplicated about once every 100 million years. The present paper speculates that the antifreeze gene evolved in response to cooling temperatures in the Antarctic deep ocean water over the past 50 million years. What are we to make, then, of the fact that Antarctic eelpouts have over 30 AFPIII genes, all of which are said to have resulted from a duplication of a single AFPIII gene which evolved at some point in the past 50 million years in response to changing ocean temperatures? http://www.evolutionnews.org/2011/01/a_fishy_story_about_antifreeze043141.html
Clue or Clueless on Plant Evolution - August 2011
Excerpt: The researchers also looked at the impact of these networks on evolution. The protein products of duplicated genes, for example, might be expected to take on different functions, as one can maintain the original task while the other is free to accumulate mutations. But the researchers found that most gene duplicates in Arabidopsis tended to interact with many of the same proteins, even though those duplicates had originated more than 700 million years ago, suggesting that the interactome somehow reduces the freedom of duplicated proteins to diverge.
Along that line of ‘tinkering’:
Evolution Everyone Can Agree On
The story concerned a hybrid plant introduced to America that underwent a spontaneous doubling of its genes. Before, the hybrid experienced relaxed gene expression, but after the doubling, expression was regained, the plants became vigorous again, and started to spread.
“No one had extended this to natural populations and the rapidity at which this can occur, and that’s pretty astonishing,” a researcher from Iowa State University remarked. Another considered this like nature hitting a “reset button” after gene expression had been disturbed by hybridization. This is an example of down-and-back-up evolution; even so, the hybrid was introduced on purpose by breeders and does not represent a natural state.
Does Gene Duplication Perform As Advertised?
The origin of biological information and the higher taxonomic categories, Stephen C. Meyer, 2004
,,,the probability of randomly assembling (or “finding,” in the previous sense) a functional sequence (for a duplicate gene) is extremely small.
Jonathan Wells Hits an Evolutionary Nerve:
"duplicating a gene doesn’t increase information content any more than photocopying a paper increases its information content."
"If you count copies as new information, you must have a hard time with plagiarism in your classes. All that the miscreant students would have to say is "It's just like gene duplication. Plagiarism is new information -- you said so on your blog!"
Professor of Neurosurgery Michael Egnor in a response to P.Z. Myers
Does Gene Duplication Increase Information Content?
"merely citing gene duplication does not help one understand how Darwinian evolution can produce new genetic information."
“The theory of gene duplication in its present form is unable to account for the origin of new genetic information”
Ray Bohlin, (PhD. in molecular and cell biology)
“Evolution through random duplications”... While it sounds quite sophisticated and respectable, it does not withstand honest and critical assessment” John C. Sanford; Genetic Entropy 2005
Asking the Right Questions about the Evolutionary Origin of New Biological Information - Feb. 2010
As we've seen, it’s easy to duplicate a gene, but the key missing ingredient in many neo-Darwinian explanations of the origin of new genetic information is how a gene duplicate then acquires some new optimized function. Evolutionists have not demonstrated, except in rare specialized cases, that step-wise paths to new function for duplicate genes exist.
John Sanford, a expert in plant genetics, examines Polyploidy (Gene/Chromosome Duplication) fallacies in Appendix 4 of his book "Genetic Entropy and the mystery of the Genome".
"What about polyploidy plants? It has been claimed that since some plants are polyploidy (having double the normal chromosome numbers), this proves that duplication must be beneficial and must increase information. Polyploidy was my special area of study during my Ph.D. thesis. Interestingly, it makes a great deal of difference how a polyploid arises. If somatic (body) cells are treated with the chemical called colchicine, cell division is disrupted , resulting in chromosome doubling - but no new information arises. The plants that result are almost always very stunted, morphologically distorted, and generally sterile. The reason for this should be obvious - the plants must waste twice as much energy to make twice as much DNA, but with no new genetic information! The nucleus is also roughly twice as large, disrupting proper cell shape and cell size. In fact, the plants actually have less information than before, because a great deal of the information which controls gene regulation depends on gene dosage (copy number). Loss of regulatory control is loss of information. This is really the same reason why an extra chromosome causes Down's Syndrome. Thousands of genes become improperly improperly regulated, because of extra genic copies.
If somatic polyploidization is consistently deleterious, why are there any polyploidy plants at all - such as potatoes? The reason is that polyploidy can arise by a different process - which is called sexual polyploidization.This happens when a unreduced sperm unites with a unreduced egg. In this special case, all of the information within the two parents is combined into the offspring, and there can be a net gain of information within that single individual. But there is no more total information within the population. the information within the two parents was simply pooled. In such a case we are seeing pooling of information, but not any new information.",,, "in some special cases, the extra level of gene backup within a polyploidy can outweigh the problems of disrupted gene regulation and reduced fertility - and so can result in a type of "net gain". But such a "net gain" is more accurately described as a net reduction in the rate of degeneration."
John Sanford - Genetic Entropy & The Mystery of the Genome - pages 191-192 - Dr. John Sanford has been a Cornell University Professor for more that 25 years (being semi-retired since 1998). He received his Ph. D. from the University of Wisconsin in the area of plant breeding and plant genetics.,,, His most significant scientific contributions involved three inventions - the biolistic ("gene gun") process, pathogen-derived resistance, and genetic immunization. Most of the transgenic crops grown in the world today were genetically engineered using the gene gun technology developed by John and his collaborators. (Due to such a stellar record in plant genetics, I take Dr. Sanford's unmatched experimental experience of plants, strictly obeying the principle of Genetic Entropy, with never a violation, to be 'state of the art' for what we can expect for the polyploidy of plants).
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