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Defending the Christian Worlview, Creationism, and Intelligent Design

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Defending the Christian Worlview, Creationism, and Intelligent Design » Theory of evolution » Gene duplication

Gene duplication

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1Gene duplication Empty Gene duplication Sat Feb 01, 2014 12:37 pm


Gene duplication

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 [3], 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???'

Related note:

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?

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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2Gene duplication Empty Re: Gene duplication Sun Feb 23, 2014 1:04 pm


The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations

it has been shown that the process of gene duplication and recruitment, as a source of evolutionary novelty, is extremely limited

In many cases, however, attempts to demonstrate the corresponding functional transitions in the laboratory require more than six base changes to achieve even weak conversions (see, for example, references 28–30). Al-though studies of this kind tend to be interpreted as supporting the Darwinian paradigm, the present study indicates otherwise, underscoring the importance of combining careful measurements with the appropriate population models.

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3Gene duplication Empty Re: Gene duplication Sat Mar 15, 2014 6:43 am




All life depends on the biological information encoded in DNA with which to synthesize and regulate various peptide sequences required by an organism's cells. Hence, an evolutionary model accounting for the diversity of life needs to demonstrate how novel exonic regions that code for distinctly different functions can emerge. Natural selection tends to conserve the basic functionality, sequence, and size of genes and, although beneficial and adaptive changes are possible, these serve only to improve or adjust the existing type. However, gene duplication allows for a respite in selection and so can provide a molecular substrate for the development of biochemical innovation. Reference is made here to several well-known examples of gene duplication, and the major means of resulting evolutionary divergence, to examine the plausibility of this assumption. The totality of the evidence reveals that, although duplication can and does facilitate important adaptations by tinkering with existing compounds, molecular evolution is nonetheless constrained in each and every case. Therefore, 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.

Invariably, the people who use this as an argument never tell us the rate of duplication necessary, nor how many duplicated but silenced genes we would expect to see in a given genome, nor the needed rate of turning on and off, nor the likelihood of a new function arising in the silenced gene, nor how this new function will be integrated into the already complex genome of the organism, nor the rate at which the silenced ‘junk’ DNA would be expected to be lost at random (genetic drift) or through natural selection. These numbers are not friendly to evolutionary theory, and mathematical studies that have attempted to study the issue have run into a wall of improbability, even when attempting to model simple changes.31-33 This is akin to the mathematical difficulties Michael Behe discusses in his book, The Edge of Evolution.34 In fact, gene deletions35 and loss-of-function mutations for useful genes are surprisingly common.36 Why would anyone expect a deactivated gene to stick around for a million years or more while an unlikely new function develops?

4Gene duplication Empty Re: Gene duplication Mon Apr 21, 2014 4:57 pm


The hypothesis of gene duplication in the evolution is false!

Note ! The theory of gene duplication turned out to be false. After many years of spreading misinformation in the end
darwinists to admit it . Darwinists loudly about this assured and very quietly canceled Their claim . Why Disciovery Institute did not yet posted ? She fell fundamental hypothesis of Darwinists!

Mechanisms that offer in return Lenski already Observed. It is natural cellular bioengineering, not a "new mechanisms of darwinian"


"The observation, published Oct. 19 in the journal Science, closes an important gap in the theory of natural selection.

Scientists have long wondered how living things evolve new functions from a limited set of genes. One popular explanation is that genes duplicate by accident; the duplicate undergoes mutations and picks up a new function; and, if that new function is useful, the gene spreads.

"It's an old idea and it's clear that this happens," said John Roth, a distinguished professor of microbiology at UC Davis and co-author of the paper.

The problem, Roth said, is that it has been hard to imagine how it occurs. Natural selection is relentlessly efficient in removing mutated genes: Genes that are not positively selected are quickly lost.

How then does a newly duplicated gene stick around long enough to pick up a useful new function that would be a target for positive selection?

Experiments in Roth's laboratory and elsewhere led to a model for the origin of a novel gene by a process of "innovation, amplification and divergence." This model has now been tested by Joakim Nasvall, Lei Sun and Dan Andersson at Uppsala.

In the new model, the original gene first gains a second, weak function alongside its main activity — just as an auto mechanic, for example, might develop a side interest in computers. If conditions change such that the side activity becomes important, then selection of this side activity favors increasing the expression of the old gene. In the case of the mechanic, a slump in the auto industry or boom in the IT sector might lead her to hone her computer skills and look for an IT position.

The most common way to increase gene expression is by duplicating the gene, perhaps multiple times. Natural selection then works on all copies of the gene. Under selection, the copies accumulate mutations and recombine. Some copies develop an enhanced side function. Other copies retain their original function.

Ultimately, the cell winds up with two distinct genes, one providing each activity — and a new genetic function is born.

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.

After growing the bacteria for 3,000 generations on a culture medium without tryptophan, they forced the bacteria to evolve a new mechanism for producing the amino acid. What emerged was a tryptophan-synthesizing activity provided by a duplicated copy of the original gene.

"The important improvement offered by our model is that the whole process occurs under constant selection — there's no time off from selection during which the extra copy could be lost," Roth said.

The work was supported by the Swedish Research Council and the National Institutes of Health.
About UC Davis

UC Davis is a global community of individuals united to better humanity and our natural world while seeking solutions to some of our most pressing challenges. Located near the California state capital, UC Davis has more than 34,000 students, and the full-time equivalent of 4,100 faculty and other academics and 17,400 staff. The campus has an annual research budget of over $750 million, a comprehensive health system and 13 specialized research centers. The university offers interdisciplinary graduate study and 99 undergraduate majors in four colleges and six professional schools."


They were confident

"Gene duplication is mentioned as one example in which information and complexity in the genome can increase leading to biochemical novelty and even irreducibly complex systems. Despite this ID proponents object to gene duplication as a relevant mechanism. I will explore some of the objections and show how science has and is addressing these objections. I intend to show that the objections raised by ID proponents are mostly without merit."

"Readers of my posts know that I'm a big fan of Professor Richard Lenski, a microbiologist at Michigan State University and member of the National Academy of Sciences. For the past few decades he has been conducting the largest laboratory evolution experiment ever attempted. Growing E. coli in flasks continuously, he has been following evolutionary changes in the bacterium for over 50,000 generations (which is equivalent to roughly a million years for large animals). Although Lenski is decidedly not an intelligent design proponent, his work enables us to see what evolution actually does when it has the resources of a large number of organisms over a substantial number of generations. Rather than speculate, Lenski and his coworkers have observed the workings of mutation and selection. For this, we ID proponents should be very grateful.

In a manuscript published a few years ago in the Quarterly Review of Biology (Behe 2010), I discussed laboratory evolution results from the past four decades up to that point, including Lenski's. His laboratory had shown clearly that random mutation and selection improved the bacterium with time, as measured by the number of progeny it could produce in a given time. He demonstrated without doubt that beneficial mutations exist and can spread quickly in a population of organisms. However, once Lenski's lab eventually identified the mutations at the DNA level (a difficult task), many of the beneficial mutations turned out to be, surprisingly, degradative ones. In other words, breaking or deleting some pre-existing genes or genetic regulatory elements so that they no longer worked actually helped the organism under the conditions in which it was grown. Other beneficial mutations altered pre-existing genes or regulatory elements somewhat.[....]"

5Gene duplication Empty Re: Gene duplication Thu May 15, 2014 5:31 pm



6Gene duplication Empty Re: Gene duplication Sun Jun 22, 2014 4:37 am


Gene Duplication and the Origin of Novel Biological Information: A Case Study of the Globins

there are at least five difficulties associated with the evolution of the globins by virtue of gene duplication and divergence. These are:

The question of the adaptive value of proposed intermediates.
Complementary changes involving the regulation of gene expression.
The time constraints associated with finding a selectable function for the duplicated copy.
The fragility problem.
Problems of convergence.

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.

7Gene duplication Empty Gene Duplication Sat Jul 12, 2014 5:05 pm


Gene Duplication

It is NOT uncommon for organisms to have duplicate copies of some genes. Duplicate genes enhance existing traits as well as add to the genomic stability of an organism, but duplicate genes have also been linked to disease. While there is no lack of theories attempting to explain these phenomena, there are no definitive answers:

“Human beings can run long distances because we carry multiple copies of a gene that helps supply our cells with energy, a new study suggests. That supports the idea that endurance running gave our human ancestors an evolutionary edge…
Humans are believed to possess anywhere from 20,000 to 25,000 different genes. But in some cases, we carry multiple copies of the same gene. And the more duplicates of a gene that exist within a cell, the more protein from the gene that gets produced, according to James Sikela at the University of Colorado Health Sciences Center in Aurora, Colorado, US.
In some cases, though, having an extra copy of a gene can translate into a serious health problem.”
“Duplicate genes help humans go the extra mile,” July 30, 2007, Genome Research 10.1101/GR.6557307.
“Knocking out a gene from a genome often causes no phenotypic effect. This phenomenon has been explained in part by the existence of duplicate genes. However, it was found that in mouse knockout data duplicate genes are as essential as singleton genes …
From single-gene knockout data in A. thaliana obtained in our study and from the literature, we found that duplicate genes play a significant role in functional compensation.”
RIKEN Plant Science Center and by National Institutes of Health, “Evolutionary Persistence of Functional Compensation by Duplicate Genes in Arabidopsis,” October 29, 2009, Oxford Journals Genome Biol Evol 1 409-414.
“Scientists have discovered that a familial form of a rare bone cancer called chordoma is explained not by typical types of changes or mutations in the sequence of DNA in a gene, but rather by the presence of a second copy of an entire gene.”
National Cancer Institute, “Gene Duplication Identified in an Uncommon Form of Bone Cancer,” October 4, 2009.
“Phenotypic variation and disease phenotypes induced by duplications are more diverse and widespread than previously anticipated, and duplications are a major class of disease-related genomic variation.”
“Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease,” Annual Review of Genomics and Human Genetics, March 26, 2007.
The record holder for duplicate genes is the bacterium Epulopiscium fishelsoni, which can have up to 85,000 duplicates of its entire genome:
“A new study carried out at Cornell and published in the Proceedings of the National Academy of Sciences journal has unveiled the secret of this gigantism: it consists in the ability of the bacterium to copy its DNA up to 85,000 times. This bacterium has a DNA amount 25 times higher than the one found in a human cell.”
Cornell University, “The Secret of the World’s Largest Bacterium Revealed,” May 8, 2008,

Darwinists believe that evolution is driven by the accidental creation of duplicate genes when random mutations disrupt partial or full chromosomal duplication. When a duplicate gene ‘slips through’ the duplication process, they believe that it is free from selective pressure, which means that it can supposedly mutate without causing damage to the organism.

It is claimed that repeated genetic rearrangements caused by insertions, deletions, inversions, and translocations in a duplicate gene can eventually assemble new sequences with the necessary instructions to build new functional features.

A star is born and gene duplication is now the mechanism of choice for Darwinism!

What is the evidence for this occurring? Notice that the following ‘scientific’ article makes the claim that the “primary evidence” for this kind of gene duplication is nothing more than the “widespread existence” of duplicate genes:

”The primary evidence that duplication has played a vital role in the evolution of new gene functions is the widespread existence of gene families …
Duplicate gene evolution has most likely played a substantial role in both the rapid changes in organismal complexity apparent in deep evolutionary splits and the diversification of more closely related species. The rapid growth in the number of available genome sequences presents diverse opportunities to address important outstanding questions in duplicate gene evolution.”
Public Library of Science, “Gene Duplication: The Genomic Trade in Spare Parts,” doi:10.1371/journal.pbio.0020206, July 13, 2004.

The next research paper claims that gene duplication created a new antifreeze gene from a duplicate copy of another gene that had a similar small section of its sequence:

“We report here clear experimental evidence for EAC-driven evolution of type III antifreeze protein gene from an old sialic acid synthase (SAS) gene in an Antarctic zoarcid fish.”
University of Illinois at Urbana-Champaign, “Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict,” 10.1073/pnas.1007883107 PNAS December 14, 2010, PNAS.

What is the “experimental evidence” that supports this conclusion? Refer to S01-S08 images:

All that is apparently required now to qualify as “experimental evidence” is this:
1.Examine the genetic sequences of gene #1;
2.find a similar sequence in gene #2;
3.incrementally add, change, and delete the genetic material enough times in #2 to make it identical to gene #1;
4.claim that it all evolved through unguided naturalistic forces.

Except for the fact that it also required human intelligence, DNA sequencing knowledge and techniques, and some cleverly made images!
Also refer to “How to Play the Gene Evolution Game” :

Notice that genetic material magically reassembles exactly where needed, and each incremental step was presumed as having been ‘fixed’ within that population for some period of time before going on to the next rearrangement. The arbitrarily switching from being ‘free from selective pressure’ to suddenly being under ‘positive selection’ displays the standard schizophrenic response to evolutionary-based hypothetical scenarios. Too bad that there is NO evidence to back it up, but the standard come-back is, “It doesn’t mean it couldn’t happen!”

“A duplicated gene newly arisen in a single genome must overcome substantial hurdles before it can be observed in evolutionary comparisons. First, it must become fixed in the population, and second, it must be preserved over time. Population genetics tells us that for new alleles, fixation is a rare event, even for new mutations that confer an immediate selective advantage. Nevertheless, it has been estimated that one in a hundred genes is duplicated and fixed every million years (Lynch and Conery 2000), although it should be clear from the duplication mechanisms described above that it is highly unlikely that duplication rates are constant over time.”
Public Library of Science, “Gene Duplication: The Genomic Trade in Spare Parts,” doi:10.1371/journal.pbio.0020206, July 13, 2004.
“A major hindrance to progress has been confusion regarding the role of positive (Darwinian) selection, i.e., natural selection favoring adaptive mutations. In particular, problems have arisen from the widespread use of certain poorly conceived statistical methods to test for positive selection (1, 2). Thousands of papers are published every year claiming evidence of adaptive evolution on the basis of computational analyses alone, with no evidence whatsoever regarding the phenotypic effects of allegedly adaptive mutations.”
Austin L. Hughes, “The origin of adaptive phenotypes,” Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193-13194, Sept. 9, 2008 (internal citations removed).
They tried this ruse in 2004 with yeast (where they used the same hypothetical sequence rearrangements-see figures in article), and it was used again in 2009 with zebrafish:

“Here, we show that the yeast Saccharomyces cerevisiae arose from ancient whole-genome duplication, by sequencing and analysing Kluyveromyces waltii, a related yeast species that diverged before the duplication.”
“Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae”:
The Broad Institute, Massachusetts Institute of Technology and Harvard University, “Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae,” April 8, 2004, Nature Publishing Group.
“Scientists have suspected that spare parts in the genome—extra copies of functional genes that arise when genes or whole genomes get duplicated—might sometimes provide the raw materials for the evolution of new traits. Now, researchers report in a study published online on September 3rd in Current Biology, that they have discovered a prime example of this in fish. The researchers show that a duplicate copy of a gene involved in embryonic development has taken up a newer and decidedly less essential role in the development of fish scales …
“By ‘tweaking’ the use of one of the two copies of the fish fgfr1, the teleost order that contains zebrafish and carp have a specialized ‘toolbox’ gene that now controls adult-specific variation in form,” added Nicolas Rohner, also of the Max Planck Institute.”
Cell Press, “Spare Gene Is Fodder For Fishes’ Evolution,” September 8, 2009, ScienceDaily.
The funny thing is that they must not have been confident in either scenario because this newer antifreeze gene duplication ruse was presented as “the first clear demonstration”:
“‘This is the first clear demonstration – with strong supporting molecular and functional evidence – of escape from adaptive conflict as the underlying process of gene duplication and the creation of a completely new function in one of the daughter copies,’ Cheng said. ‘This has not been documented before in the field of molecular evolution.’”
University of Illinois at Urbana-Champaign, “Researchers show how 1 gene becomes 2 (with different functions)”, January 12, 2011, Physorg.

What is truly alarming about these made-up scenarios is that these people still believe in the outdated gene-centered philosophy and have yet to address how the necessary and complex regulatory genetic elements evolved in unison so that the new gene would be precisely regulated.

For decades, Darwinists have dismissed regulatory elements as “junk DNA” that they believed was just useless genetic remnants left over from evolutionary predecessors. It is now known that “junk DNA” makes up approximately 98.5% of DNA and it is the key to cell health and development, and primary link to disease when not functioning properly. For more information, go to:

Is it that most evolutionary-based researchers are truly ignorant of the truth, or is it that they have chosen to ignore it hoping that it will just go away?:

“For me, the most important outcome of the human genome project has been to expose the fallacy that most genetic information is expressed as proteins … In contrast to protein-coding genes, the extent of noncoding intronic and intergenic sequences increases markedly with complexity; only 1.5% of the human genome encodes proteins …
These observations suggest that we need to reassess the underlying genetic orthodoxy, which is deeply ingrained and has been given superficial reprieve by uncritically accepted assumptions about the nature and power of combinatorial control.”
John Mattick, University of Queensland, “The genomic Foundation Is Shifting,” February 18, 2011, Science Magazine Vol. 331 no. 6019 p. 874.
“Gene regulation has turned out to be a surprisingly complex process governed by various types of regulatory DNA, which may lie deep in the wilderness of so-called junk DNA that lies between genes. Far from being humble messengers, RNAs of all shapes and sizes are actually powerful players in how genomes operate. Finally, there’s been increasing recognition of the widespread role of chemical alterations called epigenetic factors that can influence the genome across generations without changing the DNA sequence itself. The scope of this ‘dark genome’ became apparent in 2001, when the human genome sequence was first published.”
Elizabeth Pennisi, “Shining a Light on the Genomen’s ‘Dar Matter’,” Science, Vol. 330 (6011):1614, December 17, 2010.
“In order to understand gene regulation, accurate and comprehensive knowledge of transcriptional regulatory elements is essential.”
Michael Zhang Lab, Cold Spring Harbor Laboratory.
“The commercial media is both ignorant of and blocks coverage of stories about non-centrality of the gene because its science advertising dollars come from the gene-centered Darwin industry …
Thus, the public is unaware that its dollars are being squandered on funding of mediocre, middle-brow science or that its children are being intellectually starved as a result of outdated texts and unenlightened teachers.”
Suzan Mazur, “Altenberg 16: An Exposé Of The Evolution Industry” an E-Book in 8 Parts – Part 1, July 6, 2008.
Examples of regulatory mechanisms are specialized molecular switches that turn genes ‘on’ and ‘off’ at specific intervals so that genes are expressed properly. If gene duplication is a random event, it’s absurd to even suggest that these complex “highly complex, sophisticated regulatory mechanisms” evolved at the same time in order to regulate the new gene’s function:

“The cell uses highly complex, sophisticated regulatory mechanisms to make sure that not all genes are read at the same time. Particular gene switches need to be activated and, in addition, there are particular chemical labels in the DNA determining which genes are transcribed into RNA and which others will be inaccessible, i.e. where the book literally remains closed. The biological term for this is epigenetic gene regulation…
More than half of our genetic material is transcribed into noncoding RNA. This prompts Ingrid Grummt to speculate: ‘It is very well possible that there are exactly matching noncoding RNA molecules for all genes that are temporarily silenced. This would explain how such a large number of genes can be selectively turned on and off.’”
Helmholtz Association of German Research Centres, “A mystery solved: How genes are selectively silenced,” October 18, 2010, Physorg.
“The ability of cells to work together in a co-ordinated fashion is paramount for a multicellular organism to function. The multitude of cell types each have specialised roles to play, yet remain dependent upon the products of other cells for survival. Even the needs of individual cells can change according to their stage of development and environmental conditions. Multicellular organisms had to develop complex systems of control in order to regulate the different processes going on in different cells at different times. For such a system to work, there must be a sophisticated means of communication between cells. GPCRs (G protein-coupled receptor) and their G proteins (guanine nucleotide-binding proteins) form one of the most prevalent signalling systems in mammalian cells, being involved in the control of nearly every aspect of physiology and behaviour.”
Jennifer McDowall, “G Proteins,” InterPro database, European Bioinformatics Institute.

8Gene duplication Empty Re: Gene duplication Sun Jan 11, 2015 8:12 am



Please provide a detailed account of how a duplicate copy of a gene can evolve into an entirely new gene, and then can start to perform a new function.

natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone--random variation--must do the work of information generation--that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or "finding," in the previous sense) a functional sequence is extremely small.

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