". . .any and all adaptive change you can point to. NONE of them originate from a true mutational event (random chance, replication-dependent copy errors), they all originate from genomic mechanisms reacting to the outside environment."
Well, that raises a few questions. For example, if there is some mechanism to (for example) repair the
his operon, as in the Ames test, why doesn't it take place in all the bacteria that find themselves short of histidine and having a broken
his operon --- why, instead, does it take place at such low rates as to be consistent with this event being caused by chance?
(We might ask similar questions about, for example, Lenski's bacteria. If the evolution of citrate-eating bacteria is induced by a mechanism for doing so, then why did only one of the strains evolve it?)
Why is the rate of repair raised by the presence of mutagens, which are also known to increase the rate of
harmful mutations as well?
What the heck
is the mechanism? In the case of the Ames test, the mechanism must somehow "know" what the [i]his[/h] operon ought to look like. This information is stored once on the genome
in the his
operon, but when the operon is broken, it isn't there any more. Where, then, is the backup copy stored?
And it's not just repairing broken genomes that this mechanism can do. It can adapt organisms to a wide range of conditions not found in nature. So in the case of the Lenski experiments, there must have been this mechanism sitting in
E. coli, unused, waiting to spring into action when Lenski created the artificial environment in which the adaptation would be useful. What mechanism caused this adaptation, and where in the cells was the information stored as to what the genome should look like in the case that some scientist introduced the bacteria to the appropriate environment?
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As for his proposal to alter the English language, I think it would be confusing and inconvenient.
Edited by Dr Adequate, : No reason given.
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