Silent mutations are mutations which do not change the amino acid of the protein. Since the genetic code is degenerate, more than one triplet codes for the same amino acid, mutations in the genetic code can have no impact on the amino acid and thus the protein. In other words, silent mutations should not change the function of the protein and are thus considered to be evolutionary 'neutral'. But as Wikipedia explainsWe propose that the way in which some proteins fold is affected by the rates at which regions of their polypeptide chains are translated in vivo. Furthermore, we suggest that their gene sequences have evolved to control the rate of translational elongation such that the synthesis of defined portions of their polypeptide chains is separated temporally. We stress that many proteins are capable of folding efficiently into their native conformations without the help of differential translation rates. For these proteins the amino acid sequence does indeed contain all the information needed for the polypeptide chain to fold correctly (even in vitro, after denaturation). However, other proteins clearly do not fold efficiently into their native conformation in vitro. We argue that the efficiency of folding of these problematic proteins in vivo may be improved by controlled synthesis of the nascent polypeptide.
In other words, mutations which appear to be neutral, since they still code for the same amino-acid and thus the same protein, are not always neutral. The Scientist reported on December 21, 2006 that researchers had found that "Silent" mutations are not always silent" and that "Mutations leading to identical amino acid sequences can change protein folding and function". While examples of silent mutations not being silent existed in 'lower animals', this was the first time that an example was found for mammals. The study was published in Science Express Kimchi-Sarfaty C, Mi Oh J, Kim I-W, Sauna ZE, Calcagno AM, Ambudkar SV, Gottesman MM. A "silent" polymorphism in the MDR1 gene changes substrate specificity. Science Express, December 21, 2006. Compare this with the Scientific Vacuity of ID: How does Intelligent Design explain, let alone predict, this? A 'silent' mutation which nevertheless has a significant effect on the efficiency of cancer treatments.However, many organisms are known to exhibit codon usage biases, suggesting that there is selection for the use of particular codons due to translational stability. Silent mutations may also affect splicing, or transcriptional control.
16 Comments
Pigwidgeon · 2 January 2007
DaveScot said ID (or something like ID) did predict this. ;)
http://www.uncommondescent.com/archives/1901
Coin · 2 January 2007
That is interesting.
Reed A. Cartwright · 2 January 2007
When I was an undergrad, codon biases were discussed along with silent mutations. This included discussing how different codons could affect protein regulation and folding even if they didn't change the sequence. None of our professors were ID activists, yet we still discussed these things because they are part of evolutionary genetics. (Codon usage is driven by mutation and selection.) Calling the paper a prediction of ID is laughable.
Katarina · 2 January 2007
Coin · 2 January 2007
Gerard Harbison · 2 January 2007
In fact, these days, to express a protein in, say E.c oli , typically what you do is get the gene synthesized using not the native codons but a set of codons optimized for expression in E. coli . Of course, one would not expect Dave Scot to know this, any more than one would expect him to know any biological fact.
Bob O'H · 3 January 2007
k.e. · 3 January 2007
BC · 3 January 2007
Mats · 3 January 2007
Given the events in recent (and not so recent) history, "Evolutionary prediction" seems to be a term very loosely aplied to such a theory. Perhaps the best term would be "Evolutionary speculation".
Henry J · 3 January 2007
Re "Order will triumph over kaos"
With some help from Maxwell Smart of Control...
Popper's ghost · 3 January 2007
TheUsualSuspect · 8 January 2007
Gerard Harbison on 1/2/07 writes:
"In fact, these days, to express a protein in, say E.c oli , typically what you do is get the gene synthesized using not the native codons but a set of codons optimized for expression in E. coli . Of course, one would not expect Dave Scot to know this, any more than one would expect him to know any biological fact."
DaveScot on 12/24/06 writes:
"Silent mutations effecting protein folding isn't new. When researchers started sticking eukaryote genes into bacteria in quests to get cheap sources of useful enzymes they found that often the protein products ended up as insoluble inclusion bodies. They were insoluble because they didn't fold right. The also found that by modifying the gene so its codon usage was more like the host the proteins folded properly. IOW the prokaryote caulk gun (ribosome) is a bit different than the eukaryote in the way it processes redundant codons."
http://www.uncommondescent.com/archives/1901#comment-82377
Care to comment on that, Gerard? Probably not.
mike syvanen · 9 January 2007
"Care to comment on that, Gerard? Probably not."
Many people have a tendency to assume that if someone is talking real stupid then they may be uninformed. Those not familiar with DS simply assume he must be uninformed -- it is more polite to think him ignorant than blatantly dishonest.
Shawn Fahrer · 17 January 2007
Perhaps the entire concept of a "silent mutation" is faulty. And also that the concept of "the same amino acid can be coded by two different codons" is faulty in this sense: While each variant may have the same chemical formula, they could be isomers (different geometric setup-- even C6H12O6-- a common sugar-- exists in several different forms, for example. Why not amino acids, which are far more complex?) Perhaps one codon codes for one isomeric form of an amino acid, and another codes for a different isomeric form of the same amino acid. Let's check this out. While it may not "prove" ID, it may prove that our understanding of the "genetic code" is so far from complete as to be infantile....
Anton Mates · 17 January 2007