Cameron Wybrow wrote:
> Tim:
>
> Were you reading the same article that I was?
>
> Dr. Hebert wasn't talking just about the human species. He said:
>
Yes, I know.
Actually, I did the reading one better: I pulled up some scientific
articles on the subject of mitochondrial gene diversity and read them.
As I noted in my previous reply, others have confirmed that
within-species mitochondrial gene variation is often much less than
expected for neutral theory. As I explained, neutral theory mechanisms
are but a subset of evolutionary mechanisms.Other mechanisms can
predominate. It is really not a SWAG (sophisticated wild-assed guess) of
Herbert to suppose that the data reflects a selective sweep, because it
really does display those characteristics. Interestingly, it appears
that these observations generalize to the mitochondria of many species.
That suggests that there could be common mechanisms behind the phenomena
and suggests a means to investigate them.
> [...]Therefore, the results of genetic barcoding tilt more towards "creationism" than neo-Darwinism.
>
>
The results 'tilt' toward the category of 'undetermined'.
> [...]Nonetheless, Dr. Hebert rejects "creationism".
>
Good for him.
> [...] And if you reply, as you may, that new evidence for such a scouring mechanism has come up since then -- though if that's the case, please provide references rather than just asserting it -- that still doesn't change the fact that an *a priori* motive guided the initial invention of the scouring mechanism, not any evidence that one existed, or even could exist. And the *a priori* motive was to make sure that no one would come to "creationist" conclusions from data which, to a fair observer, actually suggested them.
>
>
New evidence? It's called 'selection'. There's also 'hitchiking', which
can fix unselected genes by virtue of their proximity to selected genes.
And that's just a couple of many. In the case of mitochondria, that
could cover pretty much the whole organelle's genome. A good textbook is
an excellent place to start reading about the many mechanisms that
affect genetic diversity. Still, here are some papers on the subject.
Science. 2006 Apr 28;312(5773):570-2. Bazin E, Glémin S, Galtier N.
"Population size does not influence mitochondrial genetic diversity in
animals" http://www.sciencemag.org/cgi/content/abstract/312/5773/570?ck=nck
Here's a section of a Mortiz paper from 2007:
PLoS Biol. 2004 October; 2(10): e354. C. Moritz & C. Cicero. "DNA
Barcoding: Promise and Pitfalls"
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2259444
"Over 30 years ago, Richard Lewontin concluded that intraspecific
variation is tightly constrained and recognized that both genetic drift
and natural selection offer possible explanations for this fact
(Lewontin 1974). Under genetic drift, recent population bottlenecks
could account for low intraspecific variation. It might be argued that
the low levels of mitochondrial variation detected in our study reflect
the unique history of North American birds, most of which have expanded
into their present ranges from smaller populations following retreat of
glaciers. However, restricted intraspecific mitochondrial variation also
exists in many vertebrate and invertebrate species from tropical,
temperate, marine, and terrestrial environments (Barrowclough & Shields
1984; Bucklin & Wiebe 1998; Meyer & Paulay 2005; Saunders 2005;
Hajibabaei et al. 2006), implying a more general explanation. Effective
population size for nuclear genes can reach an asymptotic limit due to
linkage; this effect is strongest for organisms with large genomes, with
the result that the effective population size of vertebrates might not
exceed 10E4 (Gillespie 2000; Lynch et al. 2006). Although not directly
applicable to mitochondria, this effect does reveal the complexities of
estimating effective population sizes and predicting the role of drift
in scouring variation.
Low mitochondrial variation might alternatively (or additionally)
reflect recurrent selective sweeps; repeated diffusions of new,
selectively favoured variants across the breeding range of a species
could purge mitochondrial diversity. Although 98% of the nucleotide
differences in COI barcode sequences in our study between nearest
neighbours were synonymous, selection on any nucleotide position in the
mitochondrial genome would result in the loss of variation in the
barcode region because mtDNA is inherited as a single linkage group, due
to its asexual transmission. Mutations in nuclear or mitochondrial loci
important in nuclear-mitochondrial co-adaptation might be particularly
important (Catalano et al. 2006). A recent analysis of patterns of
substitution in nuclear and mtDNA concluded that reduced mitochondrial
diversity in animals is due to selective sweeps (Bazin et al. 2006).
Although these authors found no correlation between census population
size and intraspecific mitochondrial variation, the range of variation
was less than expected given census population sizes. This latter
finding, together with our results showing trends toward increased
diversity in larger populations and older species, imply that genetic
drift does influence mitochondrial variation, but only weakly."
> [...] The "embarrassment to science" that I spoke of is not that evolutionary theorists consider the *possibility* of explaining biological information in terms of matter and energy alone. The embarrassment lies in their blatant a priorism, their in-advance-of-the-facts certainty that matter-energy explanations alone will be sufficient. To be willing to postulate utterly unknown mechanisms *only because if they do not exist, one's theory will be falsified or seriously weakened*, is desperate and dishonest.
Just like those developmental biologists who postulated morphogenetic
gradients before they actually discovered them? Those biologists were
overwhelmingly committed to physical mechanisms over 'interruptive'
divine intervention. I think you're actually making a general indictment
of current science.
I'm going to dig up a letter I wrote to an earlier participant on this
topic. It discussed the 'morphic resonance' hypothesis developed by
Rupert Sheldrake to explain some of the questions remaining in
developmental biology. He perceived an explanatory gap in many current
scientific explanations and tried to fill them in with a previously
unknown (by physicists), but universal mechanism. Gusty and likely
wrong, at least his mechanism had the virtue of making distinguishable,
positive predictions.
Regards,
Tim
To unsubscribe, send a message to majordomo@calvin.edu with
"unsubscribe asa" (no quotes) as the body of the message.
Received on Sat Aug 22 12:14:19 2009
This archive was generated by hypermail 2.1.8 : Sat Aug 22 2009 - 12:14:19 EDT