From: "JSeltzer"
To: <cangen@cody.library.manhattan.edu>
Date: Tue, 24 Feb 2004 14:04:07 -0500
Subject: [Cangen] Re: Evolution caught in the act
Quoting from Susan's post: "Bardwell likens the new pathway for disulfide
bond formation to engineering. 'People often speak of Computer Assisted
Design (CAD), where you try things out on a computer screen before you
manufacture them. We put the bacteria we were working on under a strong
genetic selection, like what can happen in evolution, and the bacteria
came up with a completely new answer to the problem of how to form
disulfide bonds. I think we can now talk about Genetic Assisted Design
(GAD)."
I had the opportunity this month to attend lectures by two scientists with
quite disparate takes on evolution and speciation.
Michael Behe, a professor of biochemistry at Lehigh University, spoke on
"Darwin's Black Box" and what he calls the Irreducible Complexity of a
number of biological mechanisms, e.g., the cascade of events that control
the clotting of blood. The absence of a single link in the chain and the
blood clotting mechanism fails resulting either in bleeding to death or
turning the organism's entire blood supply into one big clot. Behe
asserts that neo-Darwinism cannot explain the
simultaneous evolution of both fibrinogen and plasminogen (the balance of
which makes the system work). Like a mousetrap which (according to Behe)
requires all its separate components to catch a mouse, so also the
blood-clotting chain needs all its separate pieces. The mechanism is
Irreducible Complex and mutations that led to fibrinogen had to occur
simultaneously with other mutations that led to plasminogen -- a
"statistically impossible" simultaneity. Hence, Intelligent Design --
hence, an Intelligent Designer ... an attempt using molecular biology to
bring William Paley's Intelligent Design Thesis into the 21st century.
I suggested to Behe that simply because a biological structure appears to
be Irreducibly Complex (and which neo-Darwinism cannot, according to Behe,
explain) does not, by the process of eliminating a single hypothesis,
leave the only answer of Intelligent Design. Indeed, there are other
alternative hypotheses that must also be considered. I was surprised to
find that Behe was unfamiliar with the Morphogenic Field hypothesis of
Rupert Sheldrake. I was also surprised that Behe
had not made any attempt to elucidate the information pathway(s) that any
explication of the Intelligent Design thesis reasonably demands. When I
asked if intelligence (information content as the alternative to the
randomness assumed in neo-Darwinian evolution) was an intrinsic property
of matter, perhaps infused at the time of the Big Bang, he could offer no
response. IMO, a collision with an apparently inexplicable puzzle should
not halt further inquiry. A god of the gaps
is no god at all.
The other lecture was given by Niles Eldridge (the collaborator with
Stephen Jay Gould on the punctuated equilibrium theory of evolution).
Eldridge emphasized the evidence from paleontology that reveals long
periods of relatively slow changes in most species followed by short
periods with new species emerging and old species disappearing -- a long
period of stasis followed by a brief period of intense speciation driven
by abrupt environmental changes. This lecture, unlike Behe's, was well
supported by a considerable amount of evidence.
Yet, I for one am still struck by the remarkable degree of plasticity
inherent in the phylogenetic process. In the mere blink of an eye (on a
geological time scale), large numbers of new species have emerged when
driven by a major environmental shift -- simply because they must. As
reported in the referenced study, in the much shorter span of time that it
takes for a bacterial colony to either adapt or starve, a novel technique
for generating disulfide bonds emerges from
the latency of the bacterial genome -- simply because it must.
Is there something else going on here?
Jim Seltzer
Willowind Dalmatians
Date: Wed, 25 Feb 2004 16:22:41 -0500
From: "JSeltzer"
Subject: Re: sex linked traits/meiosis
Jane wrote: "I am trying to respond to something on Mastiff list about
the x factor theory...it seems that it is being applied generally to all
traits - not just sex linked. As if, "if in doubt, assume sex linked." The
question was to do with deciding to breed back to a grandparent - which
grandparent would be the better choice - paternal grandsire or the
maternal grandsire? I can't get my head around this.
Please help. Am I wrong when I think that the x factor is WAY too narrow
an approach to examining the likelihood's of which grandparent was the
most influential on his granddaughter as a whole?"
"...So back to my original question - if the original cell contains a gene
on a chromosome (other than on the x or the y) and this gene is a
recessive for a negative characteristic - shouldn't the gametes that
aquifer the x or the y have an equal chance of also acquiring this
recessive gene?"
IMO, focussing on sex-linked attributes is too narrow a view. Consider the
following categories:
http://www.genome.iastate.edu/edu/genetics/sexlim.html
"Sex traits can be categorized into three types of inheritance:
sex-limited, sex-linked, and sex-influenced.
"Sex-limited traits are traits that are visible only within one sex. For
instance, barred coloring in chickens normally is visible only in the
roosters.
"Sex-linked traits would be considered traits like sickle cell anemia
and color blindness. They are said to be linked because more males (XY)
develop these traits than females (XX). This is because the females have
a second X gene to counteract the recessive trait. Thus, the trait is
more likely to be visible in the male.
"Sex-influenced traits are autosomal traits that are influenced by sex.
If a male has one recessive allele, he will show that trait, but it will
take two recessive for the female to show that same trait. One such gene
is baldness."
Observe that sex-limited and sex-influenced traits are controlled by
autosomal genes (these can derive from either parent), but the expression
of these genes depends on the sex of the individual.
See, also,
http://webpages.marshall.edu/~adkinsda/B111OutlinesChromInhSxLink.html
Also, be aware that the expression a genetic trait can be controlled by
one parent or the other by using genomic imprinting. Methylation of a
cytosine nucleotide in the parental gamete can silence the expression of a
gene. There is some controversy on the importance of this mechanism, but
several known defects are traceable to its effects.
"Genomic imprinting can be loosely defined as the gamete-of-origin
dependent modification of phenotype. That is, the phenotype elicited
from a locus is differentially modified by the sex of the parent
contributing that particular allele."
Do a GOOGLE search for imprinting or take a look at:
http://www.genome.org/cgi/content/full/8/9/881
Jim Seltzer, Ph.D.
Willowind Dalmatians
From: "JSeltzer"
Subject: Re: population needed for breeding?
Anna wrote: "Now for the question part of the email.... What is
considered the needed population of breeding dogs, given that I'm sure out
COI is skyhigh?"
This same question came up last year on this list. I answered as follows:
~~~~start repost~~~~~~~
As I understand your question you are asking how large a population must
be to avoid the negative effects of random gene loss and loss of
heterozygosity (LOH).
By way of backgound, you should know that there is a natural and
unavoidable increase in the mean inbreeding for any finite breeding
population, the smaller the population, the faster the increase. Various
mate selection methods might cause a more rapid LOH, but random mating
(Hardy-Weinberg assumptions) will give the minimum increase in COI per
generation:
COI increase = 1/ (2N)
where N is the population size. Take away the random mating requirement
and the formula becomes:
COI increase = 1/(2Ne)
where Ne is the "effective population size"
If there are Nm breeding males and Nf breeding females in the
population, then
Ne = 4 Nm Nf / (Nm + Nf)
So what is the minimum Ne to sustain a "healthy" population? Professor
Per-Erik Sundgren (Swedish University of Agricultural Sciences) proposes a
5-generation rule. The COI increase in 5 generations should be held to a
maximum of 2.5% (0.5% per generation). You might find others with their
own rules, but Sundgren's is as good as
any.
0.5% = 1/ (2Ne) or
Ne = 100
Observe that Ne is NOT the number of AKC-registered dogs. It is the
effective population size and applies only to active breeders. So if
there is only a small number of breeding males compared to the females,
the Ne will be small (limited mainly by the number of males).
Mathematicians will recognize the quantity
2 Nm Nf / (Nm + Nf) as the harmonic mean of the numbers of
breeding males and females.
~~~~~end repost~~~~~~~
Anna: "So, it has come up again- two (or more?) breeders are stating that
we have enough dogs in the US to only use Black Russian Terriers that are
cleared in hips and elbows. A total of nineteen dogs is enough? Out of
those nineteen, two dogs are unregistered, five are over eight years old
(two are over ten), effectively reducing the breeding population to
fifteen or less."
Using Ne = 15, we obtain:
COI increase = 1/30 = 3.3% per generation. N.B. this is the inevitable
generational increase in inbreeding (random mating assumptions) based on
this population size. If the breed is already inbred, then this increase
will further add to that value.
This is well above Per-Erik Sundgren's healthy population rule.
I suggest you try to find ways to enlarge the population base before
becoming overly restrictive in your selection criteria.
Regards,
Jim Seltzer, Ph.D.
Willowind Dalmatians
2) the "type" of wild animals is usually more consistent than that of
domestic
ones. The reasons for that center around the phenomenon of "genetic
buffering"
which results from and is maintained by natural selection. There has
recently
been considerable discussion on this list about the reasons for the
breakdown of
genetic buffering among domestic animals, a breakdown which leads to
greater
phenotypic variability and then to attempts by breeders to standardize
"type" by
various breeding strategies, most of which involve various degrees of
inbreeding
and result in a loss of genetic diversity within the population. We
discussed
the apparent paradox that wild animals in general have a greater genetic
diversity, but a more uniform phenotype, than domestic ones, and the
implications of that paradox for breeding policies. All of that can
be found, I
believe, in the archives of this list, and reading some of it might prove
informative ... <G>
3) the laws of genetics are the same for all animals, wild or domestic.
John
--
Dr. John Burchard
Tepe Gawra Salukis
