Home » Intelligent Design » If Darwinian Evolution Can’t Fix Broken Genes, How Can It Create New Ones?

If Darwinian Evolution Can’t Fix Broken Genes, How Can It Create New Ones?

The Darwinian model of evolution holds that one of the key mechanisms of evolutionary innovation is the duplication of genes and the subsequent divergence of one of the duplicate copies to undertake a new functional role. Because a probability of a single gene stumbling upon a significantly different (yet functionally advantageous) sequence is so small, the idea is that, following a duplication of a gene, one copy is able to retain the original function, while the other is free to explore the vast sea of combinatorial possibilities in search of some novel function. It is widely believed that a duplicate gene has no phenotypic cost or advantage associated with it – that is, it is selectively neutral. In such a state, it is thought that the gene is free to mutate, independent of selection constraints or pressure. When a previously protein-coding gene incurs deleterious mutations such that it no longer codes for a useful polypeptide, the gene is rendered a “pseudogene”. One recent paper, which recently appeared in the open-access journal, PLoS Genetics, by Kuo and Ochman, entitled “The Extinction Dynamics of Bacterial Pseudogenes”, offers a potent challenge to this view. According to the paper’s abstract: Read more >>

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22 Responses to If Darwinian Evolution Can’t Fix Broken Genes, How Can It Create New Ones?

  1. When a design is optimal, the only place for a life form to go, as far the inherent optimal information in the parent species genome is concerned, is downhill for each ‘beneficial’ adaptation away from the parent species.

  2. Here is another study, though not as ‘to the core’ as this study, which none-the-less offers strong support for the conclusion:

    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. http://www.springerlink.com/co.....4014664w8/

    further notes:

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    Testing the Biological Fitness of Antibiotic Resistant Bacteria – 2008
    http://www.answersingenesis.or.....-drugstore

    Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology
    Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution.
    http://www.evolutionnews.org/2.....s_wro.html

    List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria:
    http://www.trueorigin.org/bacteria01.asp

  3. Perhaps I’ve misread something, but the title seems to be misleading, as the study is not about the inability of mutation to fix broken genes, but rather that broken copies of genes are eliminated more rapidly than might be expected?

  4. Can’t leave this study out:

    Simulating evolution by gene duplication of protein features that require multiple amino acid residues: Michael J. Behe and David W. Snoke
    Excerpt: 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.,,,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.
    http://www.pubmedcentral.nih.g.....id=2286568

    Further notes:

    Many times evolutionists are very deceptive in saying that evolutionary processes can generate functional information, as with the duplicate gene scenario, when in fact no one has ever demonstrated a gain in functional information, above a parent species, that would violate the principle of genetic entropy. These following articles reveal some of the many elaborate ploys evolutionists have used in the past to try to deceive the public into thinking evolutionary processes can easily generate functional information:

    Assessing the NCSE’s Citation Bluffs on the Evolution of New Genetic Information – Feb. 2010
    http://www.evolutionnews.org/2.....ion_b.html

    How to Play the Gene Evolution Game – Casey Luskin – Feb. 2010
    http://www.evolutionnews.org/2.....ution.html

    The NCSE, Judge Jones, and Bluffs About the Origin of New Functional Genetic Information – Casey Luskin – March 2010
    http://www.discovery.org/a/14251

  5. “Dollo’s Law” has been around since 1890.

  6. SCheesman – The second paper I cite (Gauger et al) is about fixing ‘broken genes’ via a two-step adaptive pathway. In the case with TrpA, it was likely the energy cost involved in transcribing the gene into mRNA which resulted in the cost-cutting degradative mutation.

  7. I should say the cost-cutting selection pressure – mutations occur regardless of their effects on fitness.

  8. SCheesman – The second cited paper (Gauger et al) is concerned with cost-cutting degradative selection. In this case, E. Coli lines were unable to take a two-step adaptive pathway to ‘fix’ a broken TrpA gene. Rather, they degraded the gene, likely for the purposes of cutting the cost of transcribing it into mRNA.

  9. Thanks Petrushka @ 5,,, Dollo’s Law does fit with the topic:

    The loss of morphological traits over time, for all organisms found in the fossil record, was/is so consistent that it was made into a ‘scientific law’:

    Dollo’s law and the death and resurrection of genes:
    Excerpt: “As the history of animal life was traced in the fossil record during the 19th century, it was observed that once an anatomical feature was lost in the course of evolution it never staged a return. This observation became canonized as Dollo’s law, after its propounder, and is taken as a general statement that evolution is irreversible.” http://www.pnas.org/content/91.....l.pdf+html

    A general rule of thumb for the ‘Deterioration/Genetic Entropy’ of Dollo’s Law as it applies to the fossil record is found here:

    Dollo’s law and the death and resurrection of genes
    ABSTRACT: Dollo’s law, the concept that evolution is not substantively reversible, implies that the degradation of genetic information is sufficiently fast that genes or developmental pathways released from selective pressure will rapidly become nonfunctional. Using empirical data to assess the rate of loss of coding information in genes for proteins with varying degrees of tolerance to mutational change, we show that, in fact, there is a significant probability over evolutionary time scales of 0.5-6 million years for successful reactivation of silenced genes or “lost” developmental programs. Conversely, the reactivation of long (>10 million years)-unexpressed genes and dormant developmental pathways is not possible unless function is maintained by other selective constraints;
    http://www.pnas.org/content/91.....l.pdf+html

    Dollo’s Law was further verified to the molecular level here:

    Dollo’s law, the symmetry of time, and the edge of evolution – Michael Behe
    Excerpt: We predict that future investigations, like ours, will support a molecular version of Dollo’s law: ,,, Dr. Behe comments on the finding of the study, “The old, organismal, time-asymmetric Dollo’s law supposedly blocked off just the past to Darwinian processes, for arbitrary reasons. A Dollo’s law in the molecular sense of Bridgham et al (2009), however, is time-symmetric. A time-symmetric law will substantially block both the past and the future,”. http://www.evolutionnews.org/2.....f_tim.html

    In fact, in what I consider one of the most comprehensive studies of fossils, for a ‘kind’, over a 270 million year period, Dollo’s law (loss of morphological variation) was ‘surprisingly” observed for trilobites:

    The Cambrian’s Many Forms
    Excerpt: “It appears that organisms displayed “rampant” within-species variation “in the ‘warm afterglow’ of the Cambrian explosion,” Hughes said, but not later. “No one has shown this convincingly before, and that’s why this is so important.”"From an evolutionary perspective, the more variable a species is, the more raw material natural selection has to operate on,”….(Yet Surprisingly for the author)….”There’s hardly any variation in the post-Cambrian,” he said. “Even the presence or absence or the kind of ornamentation on the head shield varies within these Cambrian trilobites and doesn’t vary in the post-Cambrian trilobites.” University of Chicago paleontologist Mark Webster; article on the “surprising and unexplained” loss of variation and diversity for trilobites over the 270 million year time span that trilobites were found in the fossil record, prior to their total extinction from the fossil record about 250 million years ago.
    http://www.terradaily.com/repo.....s_999.html

    Evolution vs. Trilobites – Prof. Andy McIntosh – video
    http://www.metacafe.com/watch/4032589

    This following tidbit of Genetic Entropy evidence came to me from Rude on the Uncommon Descent blog:

    At one of the few petrified forests that sports ginkgo wood, I was told by the naturalist that ginkgos are old in the fossil record—they date from the Permian back when trees were first “invented”. She said that there are many species of fossilized Ginkgoaceae, but Ginkgo biloba, is the only living species left. – Rude – Uncommon Descent

  10. BA77:

    The title of this thread has nothing to do with the topic.

    Dollo’s Law is spot on. Reverse mutations are improbable. Any pre-spectified mutation is improbable.

  11. Let me explain my remark. The article cited doesn’t mention reversing changes to genes that have become non-coding.

    No biologist would expect to see a mutation reversed.

  12. Petrushka -

    Go read the second cited article – http://bio-complexity.org/ojs/.....O-C.2010.2

    J

  13. From my article…

    “But what is the significance of this paper to intelligent design, and our evaluation of the causal sufficiency of the neo-Darwinian mechanisms to produce the illusion of design in living systems? Many readers may recall the publication of a paper published this spring in the brand new journal, bio-complexity by Gauger et al. In that paper, a very similar conclusion was drawn. Gauger et al demonstrated that the process of reductive evolution was sufficient to prevent lines of E. coli from taking a simple two-step pathway to a new fitness function. In this study, a trpA gene was ‘broken’ in such a way that it could recover the ability to synthesize the amino acid, Tryptophan, by reverting only two single point mutations. The authors here also concluded that the cost of transcribing a broken gene incurs significant fitness cost, and thus its removal is facilitated by positive selection.”

  14. From my article…

    No one expects even one specific mutation to occur in a reasonable time, much less two. Dhat’s the modern understanding of Dollo’s law.

    the law is “really just a statement about the statistical improbability of following exactly the same evolutionary trajectory twice (or, indeed, any particular trajectory), in either direction.”

  15. http://www.nature.com/nature/j.....08249.html

    By studying the reversibility of evolutionary changes in protein structure and function, these limitations can be overcome. Here we show, using the evolution of hormone specificity in the vertebrate glucocorticoid receptor as a case-study, that the evolutionary path by which this protein acquired its new function soon became inaccessible to reverse exploration. Using ancestral gene reconstruction, protein engineering and X-ray crystallography, we demonstrate that five subsequent ‘restrictive’ mutations, which optimized the new specificity of the glucocorticoid receptor, also destabilized elements of the protein structure that were required to support the ancestral conformation. Unless these ratchet-like epistatic substitutions are restored to their ancestral states, reversing the key function-switching mutations yields a non-functional protein.

  16. Petrushka – You stated that the content of my article had no relevance to the title. The above quote suggests otherwise.

    The probability of a specific mutations popping up in any given lineage depends heavily on the population size and population turnover time, as well as the amount of time available.

    The whole point of the argument put forward in “The Edge of Evolution” was that changes in protein structure, which require multiple co-ordinated amino acid changes before a selectable degree of utility is reached, are effectively beyond the edge of Darwinian evolution. This conclusion sits very well with the cited Bridgham et al paper, and militates heavily against the Darwinian supposition that critical protein binding sites are likely to ‘pop up’ wherever required in systems which require multiple protein interactions such as the bacterial flagellum.

  17. Petrushka – You stated that the content of my article had no relevance to the title. The above quote suggests otherwise.

    The probability of a specific mutations popping up in any given lineage depends heavily on the population size and generation turnover time, as well as the amount of time available.

    The whole point of the argument put forward in “The Edge of Evolution” was that changes in protein structure, which require multiple co-ordinated amino acid changes before a selectable degree of utility is reached, are effectively beyond the edge of Darwinian evolution. This conclusion sits very well with the cited Bridgham et al paper, and militates heavily against the Darwinian supposition that critical protein binding sites are likely to ‘pop up’ wherever required in systems which require multiple protein interactions such as the bacterial flagellum.

  18. This conclusion sits very well with the cited Bridgham et al paper, and militates heavily against the Darwinian supposition that critical protein binding sites are likely to ‘pop up’ wherever required …

    TOE isn’t a search, doesn’t require specific mutations, and most definitely doesn’t presume that specific mutions are likely. What evolutionary biologists actually say is what I quoted in the modern interpretation of Dollo’s law.

    The fact that a function or structure exists does not imply htat it was the result of a search. There are an infinite number of possible functions that will never be found or exploited by evolution.

    The most likely result of the actual need for a specific change is death and extinction.

  19. What the title of this post is saying is that evolution PROBABLY cannot fix broken genes in light of the fact that we know damaged genes get weeded out rather quickly and much more quickly that functional ones.

    As per this quote from the paper:

    “If pseudo genes are completely functionless and their eliminations from bacterial genomes were governed by a strictly neutral process, the time since gene inactivation would not influence the probability of pseudogene removal from a genome. However, examination of pseudogene occurrence across multiple Salmonella genomes revealed deviations from a model of stochastic loss. Several independent lines of evidence, including the phylogenetic distribution of pseudogenes and the pattern of mutation accumulation, each demonstrated that newly formed pseudogenes were purged from bacterial genomes faster than neutral expectation, suggesting that they confer deleterious effects.”

    And the point is that the bad genes actually “confer deleterious effects.” However we know from the discoveries of modern genetics that the genomes of human beings work extremely efficiently to regulate and delete damaged lines codes and errors in DNA- and so it should be noted that this discussion should not be merely about what “evolution”, per se’, cannot do but in fact about what the DESIGN of the properly functioning genome CAN do.

    Self regulation and error correction are hall marks of design and the central question here is whether or not the emergence of such systems can be explained as merely the result of the combination of the mechanisms of random chance and redundent laws over time.

    It is no surpise that Meyer and most other openminded critical thinking sceintists who actually understand these matters- are at least skeptical that such means of explanation are aqdequate to account for the design of life and its SC features.

    This artical shows once again that evolution is good at destroying things, and to a lesser extent preserving some useful things- but that it rarely if ever produces anyhting both new and useful- and possibly NEVER (via its own mechanisms) restores anyhting that has already been lost- thus, if it cannot restore one small lost feature how could it built an entire organism?

    Lastly, this should open up the discussion to the central question of whether there are any “built in” mechanisms within the genomes of complex living things that actually allow for “information retriveal”- in much the same way a computer has a system restore feature. Such a system or mechanism would once again be another hall mark of what one would expect of a designed object- and then we must account for the emergence of such a design typical system- of which evolution would easily have its hands full.

  20. Lastly, this should open up the discussion to the central question of whether there are any “built in” mechanisms within the genomes of complex living things that actually allow for “information retriveal”- in much the same way a computer has a system restore feature. Such a system or mechanism would once again be another hall mark of what one would expect of a designed object…

    But isnt the original research article saying that breaks are not backed up or corrected?

    There are some unspoken things going on here. A mutation that breaks a gene happens in an individual, not all at once in an entire population. If the broken gene spreads throughout the population, the break cannot be particularly detrimental.

  21. Somewhat related article from ENV:

    Convergent Genetic Evolution: “Surprising” Under Unguided Evolution, Expected Under Intelligent Design – Luskin
    Excerpt: Neo-Darwinian evolution isn’t supposed to be goal-directed, but some force is causing the same traits–at the genetic level–to appear independently over and over again.,,,
    http://www.evolutionnews.org/2.....37781.html

  22. Some in the ID community believe that irreducible complexity (IC) can be explained by front-loading of the genome with IC genes just waiting to be turned on at the right time. The reasoning of this post would pretty much blow that theory out of the water, no?

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