Article] Complex genomes evolved by chance

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.