I've stumbled upon the archives of a Mormon Leaders' evolution mail list.
You will find their struggle with scientific fact vs. faith intriguing.
Here's the link, followed by a recent dialogue.
But first, if what I'm doing with this post offends list etiquete, I
apologize in advance and beg you not to read any further:
Well, in case anyone was wondering about the lull in the perennial
about evolution, I've been off house hunting in NJ. I'm afraid my limited
time schedule is coming back to haunt me, so I will apologize in advance if
I am unable to respond to the questions or points that have been raised. In
particular, I still need to write a post on GxE as I promised Mel.
Hopefully, I'll be able to get to that in the next few days.
Carl, in reviewing your last set of email, I've come to the conclusion that
our conversation has become pretty diffuse. There are a number of points
that I wish very much to rebut, but I am going to suppress this urge so
that we can get back on track. Instead, I'm going to focus my response(s)
on what I believe are the more important issues/problems.
Also, I think it's about time for a subject line change, don'cha think?
(been a long time since we've addressed LDS extinction :-) )
> <<The only text book that I'm know you've read in its entirety is Li's
> _Molecular Evolution_. I can't imagine why Li would discuss this at all.
> What other texts were you thinking of?>>
> My reference shelf includes books by Dawkins, Dennett, Darwin, Gould and H
> Wells/Huxley, of the ones that represent the conventional viewpoint. Both
Having a good library is important when it comes to discussing a subject as
complex as Evolution. You seem to have some good books although most of
these won't help much with your avowed interest (IMO). For instance,
_Origin of Species_, which is a marvelous book, is best appreciated in
retrospect, or if you have an instructor who can point out the gems along
the way. I'm assuming by "Dawkins" that you are referring to _Climbing Mt.
Improbable_ and/or _The Blind Watchmaker_. Fun books with a lot of flavor,
but not useful for the serious student, IMO. I'm not familiar with the H.G.
Wells text but I have a hard time believing it could serve as anything other
than commentary on early aspects of the field.
In particular, you seem to be suffering from a lack of basic, introductory
information. You could use a good genetics text, possibly a good
quantitative genetics text, and you need something in the development
category as well. I realize that this is a lot to suggest, but you aren't
going to be able to compensate for an information vacuum of this magnitude
on Eyring-L. (At the level you wish to take the argument, anyway.) No one
has the time to disgorge this much information. If you are really serious
about exploring and critiquing evolution, you really need to add a few more
books to the library. (Maybe one a year or so.)
For the basic genetic text, there are several out there. On my shelf at
work, I have one from Russell, and another from Klug and Cummings, and I
have a couple more at home. IMO, none of these stands out as far superior
to the rest. If you wish to get a book in this area, I can make some
recommendations, but you may have better luck asking Chris. For
quantitative genetics, the intro text is Falconer & Mackay, but a more
comprehensive text would be the two volume Walsh/Lynch text (only one is out
so far). However, this book is a challenge. For development, I also don't
have any recommendations. I'm most familiar with Gilbert's text, and I
wasn't too thrilled with it, but there you go.
> <<> I am not discussing skeletal evolution, I am discussing how major
> > are made in DNA, and that has been the focus all along. I need to
> > understand
> > current theory in order to ensure that my concepts are correct.
> <<Carl, if you are not interested in discussing skeletal evolution, why
> you bring up skeletal evolution in hominid (specifically upright
> I am trying to pin down a very slippery subject : can major skeletal
> be made with only one or two bp changes in DNA, or is it necessary to
> regulatory genes, regional genes and specific structural genes to explain
> such changes? I suspect the first answer is that we don't know. However
> answer I get is that it could be a single bp, because we do not know if
> more may be involved. Hanging on to such an answer seems to be reaching
> something that is strongly suspected to be misleading.
This isn't a case of either/or.
Yes, major skeletal changes can be made with single mutation events (such as
point mutation, or TE insertion, in/dels, recombination, etc.). Yes, most
of these involve regulatory genes, while probably very very few involve
structural genes (the mutants we find are almost invariable in regulatory
genes). This said, if you wanted to pin me down on exactly what we know
about the source of quantitative variation at the molecular level, I'd
probably hedge a bit. So far, what we have is a pile of anecdotal
information. I, personally, think it paints a pretty good picture (with
some fuzzy edges), but if you surveyed the data, you might reach a different
conclusion. As for the single bp mutation question, this is pretty much a
non-issue. To just briefly sketch out why this is so, I think you will
agree that a single nucleotide change in a gene can have anywhere between no
effect to total disruption of function. Therefore, a single bp mutation
will have basically the same spectrum (although not necessarily the same
distribution) of effect on a regulatory gene as a more complex mutation.
The ultimate impact of the mutant will depend on how the regulatory gene
operated (I'll come back to this later, since I don't think this is
About the only type of mutant that a single bp change probably wouldn't be
involved in is a mutation which resulted in a *novel* trait. However, keep
in mind that 99.99999999% of evolution (yes, I'm pulling this number out of
thin air :-) ) has nothing to do with novel trait formation. And I mean
this to include macroevolution as well.
So where am I getting this from? Well, I grant it's a shot from the hip, but
take a look at the tree of life and see if you don't agree. Specifically,
pick extant taxa that are related at a level higher than genus (i.e. those
that are considered to differ in the macroevolutionary sense). Now ask
yourself, how much do they differ phenotypically/developmentally? For
instance, compare sample taxa from rodentia, primates and carnivora. Dogs,
mice, humans all have the same basic organ systems. E.g., our musculature,
nervous system, vasculature, digestive track and skeletal systems are
virtually identical (apart from scaling aspects). There *are* qualitative
differences (ability to see color, for instance) but I would argue that
macroevolution is predominately about quantitative differences.
> <<He argues that irreducible complexity can't arise naturally, totally
> ignoring the many examples we have of this occurring *naturally* on
> biological levels--molecular, tissue, organelle.>>
> I recognize that you do not want to be involved in Behe, but I think this
> statement is the first one I have seen that bears upon his major point. Do
> you have some examples of such naturally occurring complex changes? IIRC,
> most of the other comments about Behe had nothing to do with this concept.
Well, this isn't the first time I've made this point. For instance, I
believe I gave a "tissue" example and an "organelle" example in the essay.
Time permitting, I will be happy to provide a few examples at the molecular
level if you wish (I'll probably talk about LuxR/LuxI since that's a really
But, just to sketch out the answer in advance, irreducible complexity
appears to arise quite commonly as a result of selection operating to reduce
redundancy that arises in molecular pathways. And redundant systems
apparently arise via well known mechanisms such as recombination, or gene
[You will notice the words "appears" and "apparently." The answer to these
sorts of questions requires some sort of phylogeny reconstruction, so
inferrence is involved.]
> Carl: <<Macroevolution deals in changes in tooth enamel, and by inference
> the type of hair the specimen grows and many other characters. In order
> a TE to result in a change in tooth enamel, it must be accompanied by>
> specific changes in the DNA. Thus multiple DNA changes are required to
> a movement of some DNA into a useable form for speciation. If these
> <<So many things were confounded here, I just didn't know what to say.
> instance: 1) You seem to have brought macroevolution into the discussion;
> why, I have no idea since we were talking about TEs as a source of
> quantitative variation. >>
> Macroevolution deals in changes to higher taxa. Paleontologists look at
Given the confusion we've experienced so far, I think I need to pick this
one nit. Please allow me to reword for clarity's sake. Macroevolution
deals in changes *between* distantly related taxa.
[You have to be careful with your wording here because one might assume you
mean that there are certain changes that occur which cause or are
characteristic of macroevolution. This would be a presumption beyond the
scope of the definition.
Macroevolution is simple a gestalt of all the differences between two taxa
that are related beyond the genus level. Some of these differences may be
recent in origin, and all of them may be (individually) small.]
> <<2) TEs do not have to be accompanied by other
> specific changes in DNA to have a phenotypic effect. >>
> Now I am confused. In our recent discussion, I understood that TEs often
> just made the changes necessary for their own survival, and that if it
> disrupted some working DNA of the host, it would almost always be
> detrimental. Are there positive phenotype effects that lead to heritable
> changes in the host?
Ok, I promised to come back to this subject above, so here it is. Key
point: an effect that is detrimental to a *gene* isn't necessarily
detrimental to a *trait*. Let's say, for instance, that the environment has
changed such that the food supply is more abundant thereby favoring larger
individuals. Now if one individual in our hypothetical population
experiences a mutation inside of a gene which normally suppresses growth
hormone early in development, that gene may not be so effective anymore. As
a result, the organism would grow to a larger size. Bad for the gene, good
for the individual.
Can you see why it is important to consider the difference between
regulatory and structural genes? It's tough to imagine a mutation in a
structural gene having anything other than a devastating effect. As such,
structural genes don't vary much at all, even between genera. For instance,
mutate fibrin or tubulin and you get soup. (See how well intracellular
transport operates, or muscles contract, or cells hold together.)
But regulatory genes are a different beast altogether. Mutate a regulatory
gene and you change the timing, location, or rate of structural gene
expression. This isn't inherently bad. Organisms can live with some pretty
profound changes in regulation. The double-wing on the dragonfly for
instance is a nice example of what happens when you fiddle with a regulatory
gene. Ever see a two headed snake or a calf? These also are examples of
very extreme regulatory changes. Granted, there are better examples for
demonstrating positive fitness effects, but this should give you some
anecdotal concept of what an organism can tolerate and survive. Different
number of vertebrae? Can do. Larger or smaller jaw? No problem. More
teeth? You bet. And because these regulatory genes are arranged in
cascades, there are some with global effects, and others with local effects.
Anyway, the distribution of mutational effects is impressive.
> <<Looking at phenotypes over a macroevolutionly timescale, we do see
> changes, but these can almost invariable be explained as accumulated
> changes. >>
> Yes, I suppose they could. Do we find such piecemeal changes in the fossil
> record, or is the explanation supposition?
I'm not a paleontologist so I can't really answer this authoritatively. My
impression is that, invariably, one of two situations occurs. Either a) the
fossil record is dense, in which case accumulated changes are demonstrable
or b) there isn't enough evidence to judge and you end up with some large
time line with no way of ordering mutants.
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