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In sci.anthropology.paleo message
news:1134227239.079556.41950@xxxxxxxxxxxxxxxxxxxxxxxxxxxx by
"johnwl4@xxxxxxx" <johnwl4@xxxxxxx> . . . :
> While reading about the spread of people through Oceania, I
> was
> referred back to an opinion by Thomas Parsons. He says the
> variation between sequences of mothers and daughters is much
> higher than would be predicted from the molecular clock. He
> refers to 'hot spots' cause this high variation. So, how was
> this resolved? Does the molecular clock just refer to an
> average? How does linkage disequilibrium come into this?
> Incidentally, why the phrase, "linkage disequilibrium" ?
> Seems
> confusing to me, as if two sites were not linked.
On mtDNA everything is linked, LD is 100%. Its only recurrent
mutations that present an alternative point of view. When there is
region specific recurrency the one hypothesis is recombination. I
would point out that recombination is probably of the abortive
nature, gene conversion, and is swapping common variants between
mtDNA types. One of the principle issues however it hypervariability
in hypervariable sites. sites which are so prone to mutation that
they are best not considered in clocking. There are in fact 100s of
molecular clocks operating simultaneous on mtDNA, fairly we can been
the positions into about 10 clockable speeds, and each speed is
scattered around the mtDNA. When one talks about mtDNA mutation then
it is an average of those rates over time. Within one or two clock
ticks ones conclusions can be very poor. Even so calibration is
between 18 and 35ky per HVR1 'tick' and this does not consider rate
variation on top of that. relative Error = Deviation/Mean. SE = SD
(Time)/(N^0.5), Mean = N(number of accumulated mutations) * cycle
length.
Increasing the number of mutational differences between two
divergent types increase the SE but never beyond the confidence of
the calibration confidence. I have estimated that gene conversion
could be altering short term estimates by 10%, over long term it may
be a primary cause of transitional fading in a population. For
example the observation of transition to tranversion rates between
chimps and humans is about 2.5:1 for HVR1, but if one looks at
individuals chimps, gorilla or human trees with lots of branches the
transition to transversion rate is 15:1 in humans (and monkeys) and
10.8:1 in chimps and gorilla. The faster evolving sites tend to be
the places where the recurrent mutations are occurring, but once a
mutation is common in a bivariant population, then that mutation
appears to become recurrent. The anti-recombination folks have failed
to explain why that is.
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