If Darwinian Evolution Can't Fix Broken Genes, How Can It Create New Ones? - Evolution News & Views

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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:

Pseudogenes are usually considered to be completely neutral sequences whose evolution is shaped by random mutations and chance events. It is possible, however, for disrupted genes to generate products that are deleterious due either to the energetic costs of their transcription and translation or to the formation of toxic proteins. We found that after their initial formation, the youngest pseudogenes in Salmonella genomes have a very high likelihood of being removed by deletional processes and are eliminated too rapidly to be governed by a strictly neutral model of stochastic loss. Those few highly degraded pseudogenes that have persisted in Salmonella genomes correspond to genes with low expression levels and low connectivity in gene networks, such that their inactivation and any initial deleterious effects associated with their inactivation are buffered. Although pseudogenes have long been considered the paradigm of neutral evolution, the distribution of pseudogenes among Salmonella strains indicates that removal of many of these apparently functionless regions is attributable to positive selection.

The researchers examine the genomes of Salmonella species, arguing that the evolution of bacterial pseudogenes is not an entirely neutral process. To the contrary, bacterial pseudogenes are often actively degraded by the forces of selection. Genes which do not code for proteins, or perform regulatory functions, is most probably due to the energetic costs of transcribing them into mRNA.

The researchers conclude that "Because all bacterial groups, as well as those Archaea examined, display a mutational pattern that is biased towards deletions and their haploid genomes would be more susceptible to dominant-negative effects that pseudogenes might impart, it is likely that the process of adaptive removal of pseudogenes is pervasive among prokaryotes." They also suggest that the principle of pseudogene reductive (cost-cutting) evolution, might extend beyond the domain of prokaryotes, based on evidence for selection on the size of introns in some eukaryotic genomes (presumably, likewise, due to the energetic costs of transcription).

In the authors' discussion of their results, they further report,

If pseudogenes 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.

Obviously, it has been known for some time that not all pseudogenes are completely functionless, and many pseudogenes are even evolutionarily conserved among diverse taxa (see, for instance, here).

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.

What, then, can we conclude? Obviously, it supports the concept -- which has been propounded by proponents of ID for some time -- that there is a significant limitation on the number of mutations a "random walk" can accumulate prior to the degradation and loss of a 'broken' gene, thus significantly curtailing the ability of the mutational "search engine" to explore and survey the vast sea of combinatorial possibilities. It also serves as a potent reminder of the causal insufficiency of the Darwinian mechanism of random mutation and natural selection to account for the origins of fundamentally new protein structural domains and functions.


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