New Peer-Reviewed Paper Challenges Darwinian Evolution
Jonathan M.
Over recent months, papers challenging key elements of Darwinian theory -- 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.
The abstract reports,
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.
The mechanism under discussion is the phenomenon of gene duplication, which occurs by means of unequal chromosomal crossovers, the retropositioning of spliced mRNA, and copying of an entire chromosome, or even an entire genome. The gene duplication paradigm, as far as the origin of evolutionary novelty is concerned, is as follows: When a gene becomes duplicated, one copy of the gene is retained for its phenotypic utility (e.g. encoding for a protein or functional RNA), while the other copy of the gene is free from selective constraint, and is thus able to mutate and 'explore' alternative combinatorial possibilities (promoted by near neutral drift), in the hope of stumbling upon something useful.
The review paper attempts to "determine the existence and extent of any novel information produced as a consequence of gene duplication." The author further remarks,
"At stake is whether there is sufficient supporting evidence that the digitally communicated instructions encoded in DNA could have been constructed through known evolutionary processes, or whether the data suggests that an alternative explanation is required as in all codified nonbiological information. Therefore, this would serve as assessing the current arguments regarding the origins of biological and genomic complexity.
The author is careful to delineate what he is describing when he speaks of "information". Carefully contrasting the information present in biological systems with mere Shannon complexity, the author defines a gain in exonic information as "[t]he quantitative increase in operational capability and functional specificity with no resultant uncertainty of outcome." He then procedes to propose means of empirically verifying the role of natural selection in the creation of novel functionality.
Bozorgmehr winds up drawing similar conclusions to those drawn by Behe in his recent Quarterly Review of Biology paper: While many mutations can, at first glance, appear to have resulted in evolutionary novelty (such as in the case of antibiotic resistance), closer inspection reveals that the selected adaptations do not, in fact, result in novel genetic components. Bozorgmehr explains that "[i]n many instances...a loss of function and regulation in a harsh or unusual environment can have a beneficial outcome and thus be selected for -- bacteria tend to evolve resistance to antibiotics in such a way through mutations that would otherwise adversely affect membrane permeability," (see Delcour 2009). One example cited in the paper concerns the acquisition of organophosphorus insecticide resistance in blowflies, which is conferred by a single amino acid substitution in a carboxyl esterase. But this insecticide resistance -- though adaptively selected -- is not a case of neo-functionalization, but rather a loss in enzyme activity (Newcomb et al. 1997).
The paper goes on to examine eight case studies of adaptive evolution which have involved gene duplication, a few examples of which I will summarize in a second post.
Jonathan M.
Over recent months, papers challenging key elements of Darwinian theory -- 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.
The abstract reports,
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.
The mechanism under discussion is the phenomenon of gene duplication, which occurs by means of unequal chromosomal crossovers, the retropositioning of spliced mRNA, and copying of an entire chromosome, or even an entire genome. The gene duplication paradigm, as far as the origin of evolutionary novelty is concerned, is as follows: When a gene becomes duplicated, one copy of the gene is retained for its phenotypic utility (e.g. encoding for a protein or functional RNA), while the other copy of the gene is free from selective constraint, and is thus able to mutate and 'explore' alternative combinatorial possibilities (promoted by near neutral drift), in the hope of stumbling upon something useful.
The review paper attempts to "determine the existence and extent of any novel information produced as a consequence of gene duplication." The author further remarks,
"At stake is whether there is sufficient supporting evidence that the digitally communicated instructions encoded in DNA could have been constructed through known evolutionary processes, or whether the data suggests that an alternative explanation is required as in all codified nonbiological information. Therefore, this would serve as assessing the current arguments regarding the origins of biological and genomic complexity.
The author is careful to delineate what he is describing when he speaks of "information". Carefully contrasting the information present in biological systems with mere Shannon complexity, the author defines a gain in exonic information as "[t]he quantitative increase in operational capability and functional specificity with no resultant uncertainty of outcome." He then procedes to propose means of empirically verifying the role of natural selection in the creation of novel functionality.
Bozorgmehr winds up drawing similar conclusions to those drawn by Behe in his recent Quarterly Review of Biology paper: While many mutations can, at first glance, appear to have resulted in evolutionary novelty (such as in the case of antibiotic resistance), closer inspection reveals that the selected adaptations do not, in fact, result in novel genetic components. Bozorgmehr explains that "[i]n many instances...a loss of function and regulation in a harsh or unusual environment can have a beneficial outcome and thus be selected for -- bacteria tend to evolve resistance to antibiotics in such a way through mutations that would otherwise adversely affect membrane permeability," (see Delcour 2009). One example cited in the paper concerns the acquisition of organophosphorus insecticide resistance in blowflies, which is conferred by a single amino acid substitution in a carboxyl esterase. But this insecticide resistance -- though adaptively selected -- is not a case of neo-functionalization, but rather a loss in enzyme activity (Newcomb et al. 1997).
The paper goes on to examine eight case studies of adaptive evolution which have involved gene duplication, a few examples of which I will summarize in a second post.
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