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in article [EMAIL PROTECTED], Robert Karl Stonjek at [EMAIL PROTECTED] wrote on 25/11/03 12:30 PM: > Genome complexity > Complex genomes evolved by chance > By Cathy Holding > > The question of whether the evolution of large and complex genomes in > complex multicellular organisms is due to natural selection or simply a > function of chance has been the subject of considerable debate. In November > 21 Science, Michael Lynch and John Conery at Indiana University argue that > the inclusion of intragenic spacers-introns-and transposons, coupled with > the increase in gene number associated with genomes of multicellular animals > and plants, were not essential for adaptive phenotypic diversification > during eukaryotic evolution, but are the result of orders-of-magnitude > reductions in population size. This process magnified random genetic drift > and prevented "purifying" natural selection from removing them (Science, > 302:1401-1404, November 21, 2003). > > "Drawing from the now enormous databases provided by full-genome sequences, > we have attempted to develop (and test) a general theoretical framework for > explaining the expansion in genomic complexity (including numbers of genes, > numbers and sizes of introns, and numbers of mobile elements) in the > transitions from prokaryotes to unicellular eukaryotes to multicellular > eukaryotes," Lynch told The Scientist in an E-mail. > > "We argue that much of the 'syndrome' of genomic complexity arose not > because of direct selection for such change but because a reduction in > population size diminishes the efficiency of natural selection against > various types of genomic insertions," he said. > > Laurence Hurst, professor of evolutionary genetics at the University of Bath > explained, "If we ask the question why might a new mutation (a point > mutation, an insertion, deletion, duplication, whatever) go from rare (which > at first it must be) to common (aka, fixation), then, in principle, there > are two answers: either selection favored it or it got there by chance > (drift)," he told The Scientist by E-mail. "If a population is huge, it will > take ages and many chance steps for a given new weakly deleterious mutation > to get to fixation. In a small population, it takes just a few lucky steps." > > The mathematics in the paper are based on the effective population size, Ne. > "Generally, if the mutation reduces fitness by a small amount(s), then it > will be eliminated if s>>1/ Ne. If s is about 1/ Ne, it stands a pretty good > chance of getting to fixation. So as Ne goes up, an ever smaller number of > slightly deleterious mutations can get to fixation by chance," Hurst wrote. > "The authors say that as organisms get big, they also have low Ne. We have > introns, but small eukaryotes do not, not because they are good for us but > because our population size is too small for us to stop them accumulating." > > Read the rest at The Scientist.com: > http://www.biomedcentral.com/news/20031124/03 > > Kind Regards, > Robert Karl Stonjek. > > I think the origins of genomic complexity are better described in this http://www.applied-evolution.co.nz/selfishH/selfish_helper.ssi But hen I would say that. -- Phillip Smith phills@(buggger).co.nz replace bugger with ihug http://www.applied-evolution.co.nz "he who is smeared with blubber has the kindest heart" -- a Greenland Eskimo adage
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