Abstract: Glenn Morton claims the observed number of genetic variations
cannot arise rapidly (say in a few thousand years). Using Glenn's own
figures, I will show that it quite plausibly can. (Don't assume anything
else about my position.)
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Glenn cites examples of high levels of genetic variation:
>There was a recent Scientific American article on the MHC
>(major histocompatibility complex) which has to do with our
>immune system, in which they listed up to 59 known alleles
>Scientific American Dec. 1993, p. 78.
>Klein, in his book, _The Natural History of the Major
>Histocompatibility Complex, (New York: 1986), p. 627
>lists locations in the mouse genome which have up to
>92 known alleles.
Glenn's examples of high genetic variation were selected by him and do not
represent typical cases. His examples all involve the (MHC) genes which are
central to the immune system. These particular genes must recognize 'self'
from 'foreign' and readily key-in on new types of foreign tissue. They do
that by rapidly mutating and recombining in an effort to find a key that
matches the foreign tissue. These genes represent a higher than usual
mutation rate, higher than usual genetic variation, and do not represent the
situation for the vast majority of genes. In short, Glenn's specific
examples were (inadvertently) chosen to favor his position.
That said, I will use his figures anyway, and show he is still mistaken. I
will show that 59 alleles (for man) and 92 alleles (for mice) is achievable
in a short time. ("Alleles" are variant forms of a gene, differing usually
by one or a few mutations.)
Glenn wrote:
>The question which needs to be addressed by those of you [flood
>theorists] who don't like the concept of an ancient flood, is
>HOW DID ALL THIS VARIABILITY IN GENOME ARISE IN LESS
> THAN 100,000 YEARS? What is really ironic is that if you believe
>that all this arose within the past 100,000 years, you believe
>in rates of evolution far faster than the evolutionists do!!!!
>So why don't you join me and become an evolutionist? :-)
Glenn asks how genetic variation can arise rapidly. One simple answer is
error catastrophe and genetic deterioration -- which are compatible with the
worldview of many creationists. This is where harmful mutations accumulate
faster than the population can be rid of them. This mechanism can easily
create genetic variation in a short time. Evolutionists often overlook this
mechanism because it conflicts (if not strongly contradicts) their
worldview. Evolutionists seek high long-term rates of *beneficial*
substitution or perhaps neutral substitution, but the plausibility of those
rates is limited by the onset of error catastrophe. The substitution rates
are limited by several factors, including the mutation rate, but when the
mutation rate gets sufficiently high then error catastrophe sets in.
It turns out that beneficial change is slow, expressed neutral change can be
somewhat faster, and harmful change is the most rapid. You can plausibly
get rapid accumulation of genetic variation, *if* you are willing to accept
that the net effect is harmful. Many creationists find that view
acceptable, but it is anathema to evolutionists.
Glenn's genetic variation argument is empty. I continually emphasize to
evolutionists that their term "genetic variation" is often ambiguous and
leads to confusion. Calculations involving genetic variation are very
different depending on whether you are speaking of helpful, neutral, or
harmful variations.
Next we examine the details of Glenn's argument. I will make the math
explicit, so you can plug in your own numbers and compare other scenarios.
Estimates of mutation rate vary somewhat, so I will here use the same figure
that Glenn uses. Glenn's post used a mutation rate of "once every 10
million duplications of a DNA molecule", so let's use that figure for
discussion sake. (That's one mutation per 1E7 nucleotide duplications.)
After the union of sperm and egg (i.e. after fertilization), mammals
duplicate the genome about 50 times before producing sperm and egg in the
next generation. Because there are fifty duplications per generation, this
increases the *per generation* mutation rate by a factor of 50. My
following argument will ignore this 50-fold increase in mutation rate,
thereby *slowing* the increase of genetic variation. This assumption
disfavors my argument and therefore makes my conclusions more compelling.
>But of course when you multiply this [mutation rate] by
>the total number of base pairs in the human body you get
>a lot of mutations each duplication.
The *haploid* mammalian genome (eg. a sperm or unfertilized egg) has around
3.5 billion nucleotides. Here is the math (2 x 3.5E9 / 1E7 = 700). That
amounts to 700 new mutations in each offspring! (A side note: If even a
substantial fraction of those are expressed, the standard model of
evolutionary genetics indicates the population would be in error
catastrophe. This, I say, is the unstated reason why evolutionists
concluded decades ago, long before we had done much genetic mapping, that a
high proportion, perhaps 97 percent or more, of the genome is inert and
functionless. By assuming a highly inert genome, they sought to make the
observed mutation rates compatible with the standard model of evolutionary
genetics. For details see my book.)
Let us assume a roughly constant effective population size of one million
adults. Some of the offspring are so mutated that they die before they can
procreate. (For example, say that on average, the species produces three
offspring per adult, and only one-third of them survive to maturity. This
eliminates the severe mutations and leaves the population size constant from
generation to generation.) Even though the severely mutated offspring were
eliminated, the remaining population has still received 700 million new
mutations each generation. (700 per individual x one million individuals)
This represents a phenomenal increase in "genetic variation".
Of that portion of genetic variation that is expressed, virtually all of it
is harmful. The severe harmful mutations usually don't survive even one
generation, but the slightly harmful mutations can linger a long time,
especially when they are recessive and their effects are masked.
Sexual reproduction mixes the new mutations around the population, and
occasionally mechanisms like inbreeding and population bottlenecks can
rapidly take them to fixation. This view, unlike the evolutionists' story,
doesn't require special pleading. Here is the difference. In this view
there is a superabundance of new harmful mutations throughout the
population, and these can easily be moved to fixation merely due to a
population bottleneck, nothing else is required. Evolutionists, on the
other hand, use a variety of (often conflicting) stories in an attempt to
increase the rate of beneficial substitution. For example, they assume
(usually silently): 1) a new beneficial mutation just fortuitously happens
to be inside a particular sub-population when a population bottleneck occurs
in that sub-population, and 2) this new beneficial mutation is not rapidly
*eliminated* by the inbreeding. (They are usually eliminated because
beneficial mutations appear nearly 'neutral' in a small population, and are
eliminated by genetic drift.) By stacking such implausible assumptions
end-to-end over countless generations, evolutionists hope to make rapid
beneficial evolution seem plausible.
(Note: A population bottleneck tends to reduce genetic variation *within*
the sub-population experiencing the bottleneck. But it also tends to
rapidly differentiate the sub-population from other sub-populations, leaving
them more genetically distinct from each other.)
>But here is the problem. Since an allele resides at the same
>location on the genome, the odds that any alteration will
>occur at say a 1000 base pair is 1 in 10,000.
Let me clarify Glenn's statement for our readers. A typical gene is 1000
nucleotides in length. With a mutation rate of one in 1E7, the typical gene
would experience one mutation in 10,000 generations.
>Some alleles require multiple substitutions. and in the past
>4000 years, there have been approximately 200 generations
>giving the odds for creating a new allele at 200/10000= .02.
Here Glenn takes a human population (with a generation length of 20 years),
and he allots 4000 years (that's 200 generations) to produce genetic
variation. Then he makes a huge mistake. In effect, he has us take one
gene and duplicate it successively 200 times with a mutation rate of one per
10000, we then have ONE instance of the gene -- the 200th grand daughter of
the original gene. Then he calculates the probability that this ONE
instance of this one gene has suffered a mutation -- it is 0.02, a two
percent chance. He goes on to claim this is too low to explain the observed
high levels of genetic variation.
But Glenn misinterpreted the situation. To see his error let's again take
the above population of one million adults. Since they are diploids, there
are two million instances of the given gene. At one mutation per 10000,
there would be 200 new mutations of that gene EACH GENERATION! In 200
generations we would expect 40000 mutations to that gene. (Using Glenn's
"two percent" figure we get the same result: 2 million x 0.02 = 40000 new
mutations.) That makes for 40 thousand different versions of the gene,
known as "alleles". Yet Glenn asked for merely 59 alleles.
(Note: That was for the case of humans. Mice have a much shorter
generation time, greater fecundity, and larger populations, so they could
easily build up higher levels of genetic variation in a given time.)
Many new harmful mutations are eliminated before they procreate into the
immediately following generation, and the above calculations already
deducted those. A large portion of the remaining 40 thousand alleles would
be eliminated by genetic drift within ten generations of their introduction.
On the other hand, though genetic drift often eliminates some alleles it
occasionally increases the frequency of others. Also, sexual reproduction
and recombination mix different mutations together and are an additional
source for the creation of unique new alleles. Further analysis of the
issue would require additional data and assumptions that are more
complicated for readers to follow. But the conclusion is clear. Glenn has
not shown the slightest implausibility in the rapid origin of observed
genetic variations.
Walter ReMine
P.O. Box 19600
Saint Paul, MN 55119