molecular genetic evidence for a multipurpose genome

As i understand it even recently duplicated genes (100% functionally redundant) are not freed from selection. This means there is no expectation of relaxed selection in genes with overlapping function and that even if the genes that masked the knokout penotype has exactly the same function they would not mutate faster. Also the poperty of genetic systems that allows component genes to be mutated and mask the phenotype seems to be interactions among unrelated genes that have their own unique role and so of course are not free to mutate.Hughes, M.K. and Hughes, A.L. (1993) Evolution of duplicate genes in a tetraploid animal, Xenopus laevis. Mol. Biol. Evol. 10, 1360—1369.Zhang, J. et al. (2002) Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nat. Genet. 30, 411—415.Wagner, A. Nature Genetics. Volume 24, Issue 4, April 2000, Pages 355-361. Robustness against mutations in genetic networks of yeast.

Hi peter B.The papers are indeed very interesting but i don't see how they falsify evolution. They suggest that the neutral theory may be partly wrong and natural selection is very important in evolution but if anything thats going back to the very oldest darwinian ideas about evolution."Essential redundant genes are genes that can be knocked out with minor/no problems but point mutations in these genes are lethal) falsifies evolutionism"There are many genes which it is better to have the gene deleted than a point mutated copy because the point mutated copy has a dominant harmful property. This can be seen in the genes for adhesion in the bacterium Helicobacter pylori. If a gene is knocked out adhesion still ocurs but it is mediated by other cell surface molecules but the mutated form of the gene gives rise to a stucture that prevents the other cell surface molecules from contacting cells therefore there is no adhesion. Other examples inlude many of the collagen related diseases in humans. This effect is often seen in genes that make subunits of protein rather like say the SRC family of nuclear receptor coactivators.I don't know how resistance to mutation in genetic networks evolves or even if it has been selected for or is an accidental property of the organisation of genes, but that doesn't mean it can't have evolved. Before all the details of the interactions involved in the resistance to mutation of even one system is known speculating on weather it could or couldn't have evolved is futile.Infect Immun 2002 Jun;70(6):3073-9. Helicobacter pylori does not require Lewis X or Lewis Y expression to colonize C3H/HeJ mice.Takata T, El-Omar E, Camorlinga M, Thompson SA, Minohara Y, Ernst PB, Blaser MJ.Mol Microbiol 2000 Mar;35(6):1530-9. Lewis X structures in the O antigen side-chain promote adhesion of Helicobacter pylori to the gastric epithelium. Edwards NJ, Monteiro MA, Faller G, Walsh EJ, Moran AP, Roberts IS, High NJ.

hi peter B.i looked up alpha actinin and found this:J Biol Chem 2002 Jul 12;277(28):25609-16 Functional synergy of actin filament cross-linking proteins. Tseng Y, Schafer BW, Almo SC, Wirtz D.which states: "The relative tolerance of cells to null mutations of genes that code for a single actin cross-linking protein suggests that the functions of those proteins are highly redundant. This apparent functional redundancy may, however, reflect the limited resolution of available assays in assessing the mechanical role of F-actin cross-linking/bundling proteins.""Our studies support a re-evaluation of the notion of functional redundancy among cytoskeletal regulatory proteins."with regards to SRC-kinase not all of the interactions are known so it's difficult to even evaluate the mechanism of redundancy let alone speculate on its origin.if you want to read about genetic networks and their resistance to mutation and its evolution Andreas Wagner has written several papers on this subject which can be found here: http://samba.unm.edu/~wagnera/Publications.html

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here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO.

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How about this:L. Chen, A. L. DeVries, and C. H. Cheng. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc.Natl.Acad.Sci.U.S.A 94 (8):3811-3816, 1997.Trypsinogen duplicated (clear molecular relics of origin) then mutated to give new benefit (resistance to freezing) to the population of these antarctic fish.You might also want to read: M. Long. Evolution of novel genes. Curr.Opin.Genet.Dev. 11 (6):673-680, 2001.

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Originally posted by Fred Williams:

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FK: On the other hand, if an individual is born with a beneficial mutation, then it is not a gain unless it is beneficial to the population as a whole? What kind of logic is that?

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Sound logic!

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So all the diverse molecular and physical features associated with sexual conflict are not new information because they only favour one sex so cannot possibly benefit the whole population?. If a dragonfly evolves new genitals that remove rivals sperm this is also no new information as it doesn't benefit and in fact harms the rivals lacking this feature?.

Hi peter B.I thought you might be interested in some references on selection at 'silent' loci:L. D. Hurst and C. Pal. Evidence for purifying selection acting on silent sites in BRCA1. Trends Genet. 17 (2):62-65, 2001.T. I. Orban and E. Olah. Purifying selection on silent sites -- a constraint from splicing regulation? Trends Genet. 17 (5):252-253, 2001.L. Cartegni, S. L. Chew, and A. R. Krainer. Listening to silence and understanding nonsense: exonic mutations that affect splicing. Nat.Rev.Genet. 3 (4):285-298, 2002.The reason selection can act at these 'silent' sites is that mutations in them affect the final protein so although they are silent with respect to the amino acids they code for they are not with respect to splicing factors. What you end up with is selection against mutations that grossly alter protein structure. Most silent mutations do not affect protein structure so there is still room for neutral evolution its just something that must be considered when examining patterns of mutation and drawing concluions from that.

How about discussing the evidence that the gene was formed by trypsinogen duplication which is strong enough to conclude that the duplication did happen. With regards to the condition 'this must be observed in the lab' i believe is commonly referred to as shifting the goalposts and since the evidence for the duplication is very strong irrelavent. The mutational process for the generation of the antifreeze properties of the genes (expansion of repeats) is also well known."New research shows that fish in the Antarctic and Arctic oceans, at opposite ends of the earth, independently evolved nearly identical antifreeze glycoproteins."
Thats some neat selective quoting, you forgot to mention: "the repetitive tripeptide coding sequences in the Arctic cod Bs3—1 AFGP gene have a very different composition"Could you clearly state exactly what you (although not evolution in the real world) require in a duplicated and diverged gene. maybe even give it its own topic.

Although the ancient examples are unobserved there is good evidence that they occured, do you disagree with the evidence for the duplications and what are your reasons for this?. The evidence could be inconclusive but that should also be possible show with reference to the evidence.Your position that "gene duplication followed by mutation" does not happen is in direct conflict with Peter Borger's who used the strong evidence for selection on duplicated genes (a high rate of nonsynonymous mutations, clearly "gene duplication followed by mutation") as evidence for his multipurpose genome theory.

hi Peter B.I was not saying you believed any specific gene had arisen through duplication just that you were aware of the large amount of research that indicates a high rate of nonsynonymous compared to synonymous mutations in duplicated genes (Kondrashov et al), something which Fred Williams claimed doesn't happen ("gene duplication followed by mutation"). I realise that you are with Fred in beleiving that duplications do not play a role in evolution beyond short term environmental response.It is clear that the majority of gene duplications are manitained as a transient response to environmental pressures (Kondrashov et al) so when the pressure is removed so is the duplication. But with regards to the antifreeze example the fish still live in cold water so the selective pressure has continued for a long time and continues today and so does the altered duplicated gene. I do not see how an expectation that random duplications are important in evolution must mean they play a role in genetic redundancies. It predicts that duplications occur at random and those that confer a selective advantage are preserved. Again referring back to the fish antifreeze gene just because it was formed from a dulication of the trypsinogen gene does not mean trypsinogen is now redundant nor would there be any expectation of redundancy. A prediction of non random duplication though is that when subject to a particular toxin for example the gene duplication that gives resistance to that toxin should occur at a higher frequency in a population than other duplications, does this happen?. Also more importantly is it an actual prediction of the MPGenome theory, because i wouldn't want to propose a test based on what i assume about MPG rather than what it actually says.with regards to gene duplication and human evolution this might be of interest:"An estimated 5% of the human genome consists of interspersed duplications that have arisen over the past 35 million years of evolution. Two categories of such recently duplicated segments can be distinguished: segmental duplications between nonhomologous chromosomes (transchromosomal duplications) and duplications mainly restricted to a particular chromosome (chromosome-specific duplications).Many of these duplications exhibit an extraordinarily high degree of sequence identity at the nucleotide level (>95%)
and span large genomic distances (1—100 kb). Preliminary analyses indicate that these same regions are targets for rapid evolutionary turnover among the genomes of closely related primates. The dynamic nature of these regions because of recurrent chromosomal rearrangement, and their ability to create fusion genes from juxtaposed cassettes suggest that duplicative transposition
was an important force in the evolution of our genome."Evan E. Eichler. Recent duplication, domain accretion and the dynamic mutation of the human genome. TRENDS in Genetics Vol.17 No.11 November 2001.F. A. Kondrashov, I. B. Rogozin, Y. I. Wolf, and E. V. Koonin. Selection in the evolution of gene duplications. Genome Biol. 3 (2):RESEARCH0008, 2002.

Hi Fred
I am sorry if i misrepresented your position, i though you denied just gene duplication was a gain of information (two copies of the same book) so therefore if there was positive selection for a particular function after duplication that would represent a gain in information as the duplicated gene would no longer be the same as the original. Would it be a gain of information if the duplicated gene had a different role from the original gene?. For example supposing the antifreeze gene was formed from a duplicated trypsinogen gene as the evidence suggests would that fit your definition of an increase in information?.The examples are not just speculation but based on clear evidence, what conclusions would you draw from the evidence and how are the conclusion of the authors of the papers wrong?.