News: Evolution Of A Beneficial Mutation.
Ye Old One
By: Bradley Fikes � January 3rd, 2010
http://www.nctimes.com/app/blogs/wp/?p=6339
Evolutionary biologist Richard Lenski has demonstrated evolutionary
methods in computer models and long-running breeding programs with the
bacterium E. coli. A new paper he co-authored documents the evolution
of a particular beneficial mutation, and why it doesn�t always arise.
The paper http://www.biomedcentral.com/content/pdf/1471-2148-9-302.pdf
(PDF), published in the open access journal BMC Evolutionary Biology,
described the evolution of 12 populations of E. coli through 20,000
generations. One of them contained bacteria with a known beneficial
mutation called BoxG1, found to give a 5 percent advantage over other
E. coli without the mutation. The other 11 didn�t have the mutation.
They were all grown in the same environment.
The population with the beneficial mutation evolved so it went from
rare to universal. The 11 populations without the mutation never
evolved the BoxG1 mutation, throughout the 20,000 generations.
However, they did increase their fitness by about the same proportion
as those with that mutation. The authors say:
�It is interesting to consider two alternative hypotheses for why a
BoxG1 mutation was substituted in only one of 12 replicate
populations, despite its substantial advantage in the ancestral
genetic background. According to one hypothesis, there have not been
enough cell generations in each population for the same mutation to
have occurred in the other populations. According to the other
hypothesis, different mutations were substituted in the replicate
populations that rendered this particular mutation no longer
advantageous. The former hypothesis captures the idea of chance in its
simplest sense of individual stochastic events. The latter explanation
adds historical contingency, such that the likelihood of a particular
outcome is conditional on whether some other event has already
occurred.�
In other words, the other 11 populations may have evolved through
different beneficial mutations to the same outcome, in terms of
increased survival. If that is true, then there would be no
evolutionary pressure in the 11 populations to evolve a mutation that
would be superfluous or perhaps even harmful.
Lenski and the other authors present evidence in the article against
the first hypothesis, that there weren�t enough generations to produce
the beneficial mutation in the 11 other populations.
How can we explain its absence from the other populations? The best
explanation, in our view, relies on the effects of clonal interference
and epistasis, which together give rise to the historically contingent
form of chance. In an asexual population, such as in the long-term
experiment, two clones that acquire different beneficial mutations
will compete with one another, and only one can ultimately prevail.
Owing to this clonal interference, many beneficial mutations that
escape drift nonetheless will be lost in competition with superior
mutations.
The authors also note that while some other mutations occurred in just
one of the 12 populations, some adaptive changes elsewhere in the E.
coli genome repeated themselves in multiple populations:
�In striking contrast to these unique events, however, many changes in
the evolving populations involve repeated beneficial mutations in the
same genes. Taken together, these cases nicely demonstrate that
adaptation by natural selection can be both predictable and
unpredictable in the same experiment.�
--
Bob.
Desertphile
wrote:
> Evolution Of A Beneficial Mutation
> By: Bradley Fikes � January 3rd, 2010
>
> http://www.nctimes.com/app/blogs/wp/?p=6339
>
> Evolutionary biologist Richard Lenski has demonstrated evolutionary
> methods in computer models and long-running breeding programs with the
> bacterium E. coli. A new paper he co-authored documents the evolution
> of a particular beneficial mutation, and why it doesn�t always arise.
Also beautifully explained by Richard Dawkins in his book
"Greatest Show on Earth."
--
http://desertphile.org
Desertphile's Desert Soliloquy. WARNING: view with plenty of water
"Why aren't resurrections from the dead noteworthy?" -- Jim Rutz
rmj
> Evolution Of A Beneficial Mutation
>
> http://www.nctimes.com/app/blogs/wp/?p=6339
>
> Evolutionary biologist Richard Lenski has demonstrated evolutionary
> methods in computer models and long-running breeding programs with the
> bacterium E. coli. A new paper he co-authored documents the evolution
>
> The paper http://www.biomedcentral.com/content/pdf/1471-2148-9-302.pdf
> (PDF), published in the open access journal BMC Evolutionary Biology,
> described the evolution of 12 populations of E. coli through 20,000
> generations. One of them contained bacteria with a known beneficial
> mutation called BoxG1, found to give a 5 percent advantage over other
> They were all grown in the same environment.
>
> The population with the beneficial mutation evolved so it went from
> rare to universal. The 11 populations without the mutation never
> evolved the BoxG1 mutation, throughout the 20,000 generations.
> However, they did increase their fitness by about the same proportion
> as those with that mutation. The authors say:
>
> BoxG1 mutation was substituted in only one of 12 replicate
> populations, despite its substantial advantage in the ancestral
> genetic background. According to one hypothesis, there have not been
> enough cell generations in each population for the same mutation to
> have occurred in the other populations. According to the other
> hypothesis, different mutations were substituted in the replicate
> populations that rendered this particular mutation no longer
> advantageous. The former hypothesis captures the idea of chance in its
> simplest sense of individual stochastic events. The latter explanation
> adds historical contingency, such that the likelihood of a particular
> outcome is conditional on whether some other event has already
>
> In other words, the other 11 populations may have evolved through
> different beneficial mutations to the same outcome, in terms of
> increased survival. If that is true, then there would be no
> evolutionary pressure in the 11 populations to evolve a mutation that
> would be superfluous or perhaps even harmful.
>
> Lenski and the other authors present evidence in the article against
> the beneficial mutation in the 11 other populations.
>
> How can we explain its absence from the other populations? The best
> explanation, in our view, relies on the effects of clonal interference
> and epistasis, which together give rise to the historically contingent
> form of chance. In an asexual population, such as in the long-term
> experiment, two clones that acquire different beneficial mutations
> will compete with one another, and only one can ultimately prevail.
> Owing to this clonal interference, many beneficial mutations that
> escape drift nonetheless will be lost in competition with superior
> mutations.
>
> The authors also note that while some other mutations occurred in just
> one of the 12 populations, some adaptive changes elsewhere in the E.
> coli genome repeated themselves in multiple populations:
>
> the evolving populations involve repeated beneficial mutations in the
> same genes. Taken together, these cases nicely demonstrate that
> adaptation by natural selection can be both predictable and
>
I missed it. How is it predictable?