Peter citing Hickson and Cann write:
"The mean sequence difference among alleles within a lineage corresponds
to an average age of 180,000-320,000 years (range based on the standard
error). This implies that the vast majority of the more than 135
contemporary HLA-DRB1 alleles have a very recent origin." ... "Because
the ARS and non-ARS codons do not share the same evolutionary history,
... a realistic estimate of the age of alleles cannot be obtained using
exon sequences."
and
"The coalescence time of alleles within allelic lineages indicates that the
effective population size (Ne) for early hominids (over the last 1 Myr) was
approximately 10^4 individuals, similar to the estimates based on other
nuclear loci and mitochondrial DNA. "
I do thank you for these and I have ordered them. Now, lets assume that the
above is correct. First, it means that all views in which Adam and Eve are
less than 300,000 years are wrong. One must use the older coalescence time
to date the species because as new alleles arise, they occur after the
speciation event and can't be used to date such an event. Later allele
generation merely means that the speciation event was prior to the
coalescence time.
Secondly, by apologetical standards, 320,000 years is not 'very recent'. It
represents an older estimate for Adam and Eve than any apologist other than
me.
Thirdly, an effective population size of 10,000+ people for the past million
years certainly doesn't fit the traditional idea of Adam and Eve being
created within the past 60,000 years.
As to evidence of genetic continuity one can cite the fascinating case of
green opsin in the eye.
"Two recent molecular studies favor some degree of regional continuity over
complete African replacement. The first study concerns polymorphisms in the
genes for green and red visual pigments. Color vision in animals is
mediated by light-sensitive pigments consisting of a chromophore covalently
linked to a protein moiety (opsin). The genes coding for opsins in the red
and green pigments are located on the long arm of chromosome X, whereas the
one for the blue pigment is on chromosome 7. In humans, the red and green
opsin genes are highly homologous and consist of six exons. The duplication
of these two genes has been dated to 30-40 Myr B. P., shortly after the
divergence of the Old-and New-World primates.
"The green and red opsin genes have now been sequenced in a sample of 16
chimpanzees, 7 gorillas, and 4 orangutans, yielding a total of 14 biallelic
polymorphic sites (all in either exon 2 or 4). Six of these polymorphisms
are also found in humans, which indicates that they are of ancient origin
predating the divergence of humans and apes.
"One of these trans-specific polymorphisms involves the amino acid residue
65, which in the green opsin gene of orangutans and humans can be either
threonine or isoleucine. The relevant results is that this polymorphism has
been found in Caucasians (the Ile-65 allele in 4 out of 120 individuals) but
not in a sample of 56 individuals of African ancestry and 49 of Asian
ancestry. It is possible that the Ile-65 allele may eventually be found in
African populations. It is also possible that it may have been lost from
African and Asian populations in recent times, that is, after the emergence
of modern humans. But since this polymorphism is millions of years old,
loss of the allele over the long period since the migration of H. erectus
out of Africa is more likely than a recent loss. In the replacement model,
migrants from Africa colonize other parts of the world and replace any
preexisting populations within the last 200,000 years. It would seem
unlikely that the polymorphism would have been passed on to Caucasian
populations and become thereafter lost in the larger African population.
Thus, the opsin polymorphism argues (mildly) against a complete replacement
of the Caucasian gene pool by African populations.
"The second example concerns an autosomal recessive disorder in lipid
metabolism due to the absence of apolipoprotein C-II, the physiological
activator of lipoprotein lipase, a key enzyme in very low density
lipoprotein metabolism. Two deleterious alleles, one from a Venezuelian
Caucasian family and one from a Japanese family, share a frameshift mutation
suggesting common ancestry. These two mutants diverged from the normal
allele at least 2 Myr B. P. The persistence of two defective alleles over
such a long time is a puzzle, perhaps a consequence of small heterozygote
advantage. But this persistence (i) argues against extremely small
population bottlenecks throughout the Pleistocene human history, and (ii)
favors the conclusion that European and Asian H. erectus have contributed
to the gene pool of modern H. sapiens." ~ Francisco J. Ayala, Ananias
Escalante, Colm O'hUigin and Jan Klein, "Molecular Genetics of Speciation
and Human Origins," Proc. Natl. Acad. Sci, USA, 91:6787-6794, July 1994, p.
6793.
And we can also cite the case of other nuclear polymorphisms
“For most polymorphisms tested so far, humans share a single
allele with other primates; such shared alleles are likely
to be ancestral.” Joanna L. Mountain, et al, “Evolution of
Modern Humans: Evidence from Nuclear DNA Polymorphisms,” in
Mi. I. Aitken, C. B. Stringer, and P. A. Mellars, The Origin
of Modern Humans and the Impact of Chronometric Dating,
(Princeton: Princeton University Press, 1993), pp 69-83,
p. 69
**
“Humans have been found to share a polymorphism (at least two
shared alleles at a genetic locus) with one of these closely
related species in only two cases; they share one
polymorphism with chimpanzees and another with orangutans.
For many other polymorphisms, however, humans share exactly
one allele with other primates. These shared alleles
indicate sequence similarity for a small stretch of DNA.
Considering those 71 polymorphisms for which all three of
the non-human primate species have been tested, in 57 out of
71 cases chimpanzees and humans share a single allele, in 39
out of 71 cases gorillas and humans share one allele, and in
41 out of 71 cases orangutans and humans share one allele.”
Joanna L. Mountain, et al, “Evolution of Modern Humans:
Evidence from Nuclear DNA Polymorphisms,” in M. I. Aitken,
C. B. Stringer, and P. A. Mellars, The Origin of Modern
Humans and the Impact of Chronometric Dating, (Princeton:
Princeton University Press, 1993), pp 69-83, p. 76
**
“The suggestion of an African origin for humans could
reflect a migration out of Africa either 1-1.5 Ma ago, 100
ka ago, or both. Nuclear genetic data alone provide no
timescale.” Joanna L. Mountain, et al, “Evolution of Modern
Humans: Evidence from Nuclear DNA Polymorphisms,” in M. I.
Aitken, C. B. Stringer, and P. A. Mellars, The Origin of
Modern Humans and the Impact of Chronometric Dating,
(Princeton: Princeton University Press, 1993), pp 69-83, p.
79
And then there is mtDNA insertions into the nuclear genome which show that
modern humanity has a connection back to the time of Homo erectus:
AD=Alzheimer's disease
“Regardless of the origin of the putative AD missense mutation mtDNAs, the
nuclear CO1 and CO2 sequences reported in this study are interesting in
their own respect. They were transferred from the mtDNA to the nucleus long
after the hominid lineage separated from the chimpanzee and gorilla
lineages. Because the time of insertion of the sequence into the nucleus is
estimated to be about 770,000 years before present, the transfer of these
sequences might have occurred in archaic Homo.” Douglas C. Wallace, et al,
“Ancient mtDNA sequences in the Human Nuclear Genome: A Potential Source of
Errors in Identifying Pathogenic Mutations,” Proc. Natl. Acad. Sci.,
94(1997):14900-14905, p. 14905
and
“The potential for such a scenario is underscored by the estimation that
there are approximately 1000 mtDNA-derived sequences integrated into the
human nuclear genome. Because most of these mtDNA sequences have been
integrated into the nuclear genome before the origin of anatomically modern
humans, these sequences will contain phylogenetically ancient nucleotide
sequence variants that may be inadvertently interpreted as pathogenic
variants.” Douglas C. Wallace, et al, “Ancient mtDNA sequences in the Human
Nuclear Genome: A Potential Source of Errors in Identifying Pathogenic
Mutations,” Proc. Natl. Acad. Sci., 94(1997):14900-14905, p. 14904
**
**
No matter how we cut things, whether by means of the MHC genes, by opsin,
other polymorphisms or mtDNA insertions the genetic evidence is clear that
apologetics has a problem here that must be solved. Adam and Eve simply
can't be less than 60,000 years ago and at the same time the parents of all
humanity. No amount of denial will change this conclusion.
glenn
see http://www.flash.net/~mortongr/dmd.htm
for lots of creation/evolution information
>
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