Article] Complex genomes evolved by chance

Robert Karl Stonjek <[email hidden]> quoted:

[ Re: biomedcentral.com03Open ↗ ]

Quoted message said:

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. [...]

Quoted message 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."

If we ask the question why might a new mutation go from rare to common then, in principle, there are
at least three answers:

1. selection favored it;
2. it got there by chance;
3. It was in linkage disequilibrium with something selection *did* favour.

This isn't just a minor nitpick - the effect of the third point can be a large one.

Consider the fact that much constructive evolution takes place by duplication and then variation of
one of the copies. If a variation in one of the copies proves beneficial, then the rest of the
duplicated section can be dragged along for the ride - through virtue of being linked to it.

Linkage is at its strongest when we are talking about whole chromosomes - where there is no easy way
for unlinking to happen - but can be a substantial factor elsewhere.
--
__________
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in article [email hidden], Robert Karl Stonjek at
[email hidden] wrote on 25/11/03 12:30 PM:

Quoted message said:

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: biomedcentral.com03Open ↗

Kind Regards, Robert Karl Stonjek.

I think the origins of genomic complexity are better described in this applied-applied-Open ↗
evolution.co.nz/selfishH/selfish_helper.ssi

But hen I would say that.

--

Phillip Smith phills@(buggger).co.nz replace bugger with ihug applied-evolution.co.nzapplied-evolution.co.nzOpen ↗

"he who is smeared with blubber has the kindest heart" -- a Greenland Eskimo adage

Quoted message said:

"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."

This theory kind of grows on you, so to speak.

My initial reaction was, "How can small population size favor a particular direction (pro-
complexity) to evolution? And what does fixation have to do with it? After fixation, can't the
species just back-mutate to the original wild state?"

Then I realized that the real pro-complexity force is a kind of mutation pressure. Forward mutation
rates are not the same as back mutation rates. The math really says that small populations are more
susceptible to mutation pressure than large ones. Large populations need a much larger fluctuation
to fix the deleterious allele - absent such an improbable fluctuation, they can simply revert to the
wild state without having to back mutate.

Interesting.

The application to big organisms and complex genomes is just that - an application of a much more
basic idea. Why is there mutation pressure in favor of complex genomes? Phillip Smith selfishly
suggests one reason. But he doesn't need to thank me for the help.

Tim Tyler <[email hidden]> wrote in
:"]news:[email hidden]:

Quoted message said:

Robert Karl Stonjek <[email hidden]> quoted:

[ Re: biomedcentral.com03Open ↗ ]

Quoted message said:

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. [...]

Quoted message 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."

If we ask the question why might a new mutation go from rare to common then, in principle, there
are at least three answers:

1. selection favored it;
2. it got there by chance;
3. It was in linkage disequilibrium with something selection *did* favour.

This isn't just a minor nitpick - the effect of the third point can be a large one.

Consider the fact that much constructive evolution takes place by duplication and then variation
of one of the copies. If a variation in one of the copies proves beneficial, then the rest of the
duplicated section can be dragged along for the ride - through virtue of being linked to it.

Linkage is at its strongest when we are talking about whole chromosomes - where there is no easy
way for unlinking to happen - but can be a substantial factor elsewhere.

Actually No. 3 could be argued to be the same as No.2, since the linkage disequilibrium is still
due to "chance". This _is_ a nitpick - drift can only be significant in small populations while
linkage can affect much larger populations. But I do not think linkage is totally immune from
statistics - in large populations crossover will soon break the link. So potentially we have three
different ranges of effect, in small, medium and large populations. It would be nice to see if
real populations show different rates and types of gene frequency change based on effective
population size.

Yours, Bill Morse

in article [email hidden], Jim Menegay at
[email hidden] wrote on 5/12/03 2:48 PM:

Quoted message said:

Then I realized that the real pro-complexity force is a kind of mutation pressure. Forward
mutation rates are not the same as back mutation rates. The math really says that small
populations are more susceptible to mutation pressure than large ones. Large populations need a
much larger fluctuation to fix the deleterious allele - absent such an improbable fluctuation,
they can simply revert to the wild state without having to back mutate.

Interesting.

The application to big organisms and complex genomes is just that - an application of a much more
basic idea. Why is there mutation pressure in favor of complex genomes? Phillip Smith selfishly
suggests one reason. But he doesn't need to thank me for the help.

Thanks ;-) Another way of putting it is that complexity is an adaptation to a particular type of
stress . We are very familiar with adaptations to environmental and biological stress. Genetic load
places another form of stress. A plant may adapt to situations of low water availability, caused by
environmental effects, by evolving changes in its physiology, anatomy and behaviour. Then is it
reasonable to suggest it may also adapt to low water supply, due to faulty roots, caused by
mutation? This is of course a crude example but how can selection tell the difference between the
two causes of the same water stress. I had better add the it is possible of the two causes of stress
to have about the same probability. Plants would have to adapt to the one in X years drought
although few plants would ever experience a drought. Like wise they may have a similar probability
of experiencing faulty roots depending on the frequency of the gene in the population. It is of
course likely that the adaptive response may be the same in both cases
--

Phillip Smith phills@(buggger).co.nz replace bugger with ihug applied-evolution.co.nzapplied-evolution.co.nzOpen ↗

"he who is smeared with blubber has the kindest heart" -- a Greenland Eskimo adage

William Morse <[email hidden]> wrote or quoted:

Quoted message said:

Tim Tyler <[email hidden]> wrote in

Quoted message said:

Robert Karl Stonjek <[email hidden]> quoted:

Quoted message said:

Quoted message said:

[ Re: biomedcentral.com03Open ↗ ]

Quoted message said:

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. [...]

Quoted message 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."

If we ask the question why might a new mutation go from rare to common then, in principle, there
are at least three answers:

1. selection favored it;
2. it got there by chance;
3. It was in linkage disequilibrium with something selection *did* favour.

This isn't just a minor nitpick - the effect of the third point can be a large one. [...]

Actually No. 3 could be argued to be the same as No.2, since the linkage disequilibrium is still
due to "chance". [...]

Maybe - but the original quote was:

``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)," [...]

The third case I mentioned appears to be missing.

In principle, linkage may not be random - e.g. in the case where the new mutation is a modification
to an existing gene - and that has previously migrated towards the gene it is linked with (along the
chromosome) - since their phenotypes depend of each other - and they don't like being split up.
--
__________
|im |yler timtyler.orgtimtyler.orgOpen ↗ [email hidden] Remove lock to reply.