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Re: Resetting the "molecular clock hypothesis"
> However, the mastadon/mammoth case makes this rather
> irrelevant - it seems we are talking about convergent
> evolution on the molecular scale, which I haven't heard
> of before,
You never heard about long branch attraction in moecular phylogenetics? ;-)
(OK, I know that's not what you mean. But simple statistics will show molecular
convergence on the *point mutation* level pops up quite quickly in some
sequences. Consider a ~2%/Ma mutation rate for cytB commonly found in rodents
and passeriforms; statistically every base in that sequence has mutated once
between the most divergent lineages of these two, and since mutations are not
equally distributed you can expect *some* amount of convergence here to pop up).
Then we have the case of large-scale events, though it may be hard to
distinguish convergence from retained plesiomorphisms. See for example here:
"...nucleotide insertionâdeletions that support mutually exclusive
phylogenetic hypotheses in different gene trees." (they conclude that it's
retained plesiomorphies inconsistently retained through incomplete lineage
sorting). In active retroposon insertion hotspots on the other hand it is just
as likely to be convergence.
It is not common enough, but this is of little comfort when the sequence you
want to use has undergone such "not common" events. And the main drawback of
molecular data - homoplasy is probably more common in anatomy, but if the scope
of your study is not overly large (say Livezey/Zusi-large), you can tailor your
characters so that it is not that much of a problem. For sequence data where
there are just 4 possible character states and with each change of state the
previous state gets entirely obliterated, it is more problematic. So you can
prevent the "Gaviomorphae" from popping up by tricks such as not treating
cnemial crests as a binary-state (present/absent) character. But you cannot
*know* what some base position has changed from, only what it has changed to
here and now.
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