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If most molecular evolution is non-Darwinian, how can codon bias and duon codes evolve?

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Most molecular evolution is neutral. Done.

PZ Myers

From wiki:
Codon usage bias

Codon usage bias refers to differences in the frequency of occurrence of synonymous codons in coding DNA. A codon is a series of three nucleotides (triplets) that encodes a specific amino acid residue in a polypeptide chain or for the termination of translation (stop codons).

There are 64 different codons (61 codons encoding for amino acids plus 3 stop codons) but only 20 different translated amino acids. The overabundance in the number of codons allows many amino acids to be encoded by more than one codon. Because of such redundancy it is said that the genetic code is degenerate. Different organisms often show particular preferences for one of the several codons that encode the same amino acid- that is, a greater frequency of one will be found than expected by chance. How such preferences arise is a much debated area of molecular evolution.

It is generally acknowledged that codon preferences reflect a balance between mutational biases and natural selection for translational optimization. Optimal codons in fast-growing microorganisms, like Escherichia coli or Saccharomyces cerevisiae (baker’s yeast), reflect the composition of their respective genomic tRNA pool. It is thought that optimal codons help to achieve faster translation rates and high accuracy. As a result of these factors, translational selection is expected to be stronger in highly expressed genes, as is indeed the case for the above-mentioned organisms. In other organisms that do not show high growing rates or that present small genomes, codon usage optimization is normally absent, and codon preferences are determined by the characteristic mutational biases seen in that particular genome. Examples of this are Homo sapiens (human) and Helicobacter pylori. Organisms that show an intermediate level of codon usage optimization include Drosophila melanogaster (fruit fly), Caenorhabditis elegans (nematode worm), Strongylocentrotus purpuratus (sea urchin) or Arabidopsis thaliana (thale cress).

Recall selection entails a cost of maintenance and cost of construction. Has anyone bothered to estimate how expensive (in terms of reproductive excess) it is to evolve and maintain codon bias? Or how about the cost of maintenance and construction of the duon code? How about any other difficulty?

Let us suppose then that there is no budget to pay the cost of construction and maintenance of codon bias or duon codes, then we might be forced to conclude evolution of codon bias and duon codes were non-Darwinian and hence neutral, and hence a random walk. But the problem is codon bias and duon codes by definition are non-random features of the genome and thus cannot be the product of the random walks of Kimura/Nei neutral evolution.

Thus selection can’t work, neither can neutral evolution. There is of course a third option. Just sayin. 🙂

Comments
I agree. How Dual-Use Codons Challenge Statistical Methods for Inferring Natural Selection
WGalbriath, Welcome to Uncommon Descent. Thanks for the link!scordova
April 23, 2014
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More to the point, cost of substitution arguments are mostly a waste of time. But it is well known codon bias is most strong in species with large populations, where detection of strongest...wd400
April 23, 2014
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Key word there is 'most'. And "duons" aren't a thingwd400
April 23, 2014
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Nice to see wiki is up to date:
There are 64 different codons (61 codons encoding for amino acids plus 3 stop codons) but only 20 different translated amino acids.
One of my pet-peeves - 20 amino acids. Really? So who is going to break the news to selenoproteins that they are not needed (yet are pretty essential for many organisms)? And we will not even mention pyrrolysine or variants of methionine. So when is a stop codon not a stop codon? When it is another amino acid. How do you take a code that says "stop gene synthesis" and suddenly change your mind to add in a selenocysteine which is essential for your function, where it is seen present? The only thing we see with selenoproteins is LOSS - it is present from some archae to humans, but not in fungi, not in higher plants (but in algae)...it to my mind causes all sorts of weird explanations to be employed to explain its pattern evolutionarily speaking. JDDr JDD
April 23, 2014
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I agree. How Dual-Use Codons Challenge Statistical Methods for Inferring Natural SelectionWGalbraith
April 23, 2014
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How about the bioelectric code The (Electric) Face of a Frog - video https://www.youtube.com/watch?v=0VULjzX__OM Cracking the bioelectric code: Probing endogenous ionic controls of pattern formation - January 2013 Excerpt: A recent paper demonstrated that a specific voltage range is necessary for demarcation of eye fields in the frog embryo. Remarkably, artificially setting other somatic cells to the eye-specific voltage range resulted in formation of eyes in aberrant locations, including tissues that are not in the normal anterior ectoderm lineage: eyes could be formed in the gut, on the tail, or in the lateral plate mesoderm. These data challenge the existing models of eye fate restriction and tissue competence maps, and suggest the presence of a bioelectric code-a mapping of physiological properties to anatomical outcomes. http://www.ncbi.nlm.nih.gov/pubmed/23802040 Not in the Genes: Embryonic Electric Fields - Jonathan Wells - December 2011 Excerpt: although the molecular components of individual sodium-potassium channels may be encoded in DNA sequences, the three-dimensional arrangement of those channels -- which determines the form of the endogenous electric field -- constitutes an independent source of information in the developing embryo. http://www.evolutionnews.org/2011/12/not_in_the_gene054071.htmlbornagain77
April 23, 2014
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I don't follow. The last paragraph says codon bias in humans is only "determined by the characteristic mutational biases seen in that particular genome" and therefore not selection.
In other organisms that do not show high growing rates or that present small genomes, codon usage optimization is normally absent, and codon preferences are determined by the characteristic mutational biases seen in that particular genome. Examples of this are Homo sapiens (human) and Helicobacter pylori.
JoeCoder
April 23, 2014
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