Well Dr. Davison! A hearty thanks for finally engaging in scientific discussion after much dodging on your part. But first I wanted to mention that I do indeed have not only a penis, but two glorious testicles, and thus your attempts to feminize me are unwarranted. (And as an aside, I checked out your photo at your website, and must say your skin also has a pinkish hue! We are not all that different, you and I!)
As an aside, I am glad to hear that we have at least a small audience - though I love, simply love, the fact that even when presented with a proper name, rather than an alias, you refuse to believe the name to be true! Even proper names appear as aliases to you! Why bother worrying about such, Dr. Davison? Please simply address the merits of the arguments, rather than childishly chide character of which you know not.
Also, you seem to imply that I am uninterested in interaction with you - simply not true - I do not have the luxury of being a retired philospher such as yourself, and was hard at work at the bench for the past nine hours, and thus can not be nearly as attentive as you towards this forum (the one at which you refuse to communicate).
To recap, I asked two questions, and you have now provided a response to those questions:
Dr. Sasquatch asks:
1. You make a clear distinction between allelic changes and chromosomal rearrangments, the former cannot contribute to speciation (or does so rarely), while the latter is the primary mode of speciation. My question: What is the distinction between an allelic change and a chromosomal rearrangment at the genetic level? As an example, I'm assuming you would consider a 1 Mb inversion or translocation to be a chromosomal rearrangment, but what about a 100 base pair inversion, or smaller?
Dr. Davison answers:
Well that is pretty easy. An allelic substitution is a modification of a gene. Such changes have nothing to do with evolution and at best can produce only varieties. An inversion or translocation or any other gross rearrangement of the genome need not change any genes whatsoever yet such changes obviously affect several phenotypic expressions simultaneously. Most important, such rearrangements create serious problems for the fertility of a hybrid in which one chromosome is normal and its homologue is modified. While these are minimal in effect as long as only one or a few of the chromosome complement are hererozygous, they will invariably result in sterility if several heterozygotes are invlved as in the mule for example...
Also to claim that there is a continuum beteween allelic substitutions and chromosome rearrangements is absurd. They are entirely different phenomena. While evey genetic change probably has some effect on the phenotype, only structural rarrangements have been involved in evolution. Except as they eventually can lead to extinction, point mutations in no way influence reproductive potential and so are meaningless as evolutionary devices. To continue to adhere to this gradualist view is without foundation.
Dr. Sasquatch responds:
Such a simplistic answer belies your background in physiology, and suggests a great deal of ignorance regarding molecular genetics on your part. Honestly, it seems as though you either misunderstood or intentionally side-stepped my question entirely.
I simply cannot believe you are so ignorant of basic genetics to say there is simply nothing but allelic substitution and chromosome-level rearrangment in the mutational palette!
Even at a simple logical level, you should realize that something as complex as a genome would not be mutable in such a binary way. Just off the top of head, and possibly poorly organized, is a surely-incomplete list of possible mutations in the continuum I imagine.
from "Least speciation potential"- single base substitution
- single base insertion/deletion (indel)
- microsatellite indel
- decibase-level indel
- decibase-level duplication
- decibase-level inversion
- decibase-level translocation
- kilobase-level indel
- kilobase-level duplication
- kilobase-level inversion
- kilobase-level translocation
- megabase-level indel
- megabase-level duplication
- megabase-level inversion
- megabase-level translocation
- chromosome-level indel (reciprocal)
- chromosome-level duplication (reciprocal)
- chromosome-level inversion (reciprocal)
- chromosome-level translocation (reciprocal)
- interspecific genetic exchange
- chromosome-level indel (non-reciprocal)
- chromosome-level duplication (non-reciprocal)
- chromosome-level inversion (non-reciprocal)
- chromosome-level translocation (non-reciprocal)
- full-complement ploidy changes
- aneuploidy
to "Most speciation potential"
Let me know if you have anything to add. The heart of my question, though:
Where in that range of mutations do you place the distinct boundary you speak of between "allelic substitution" and "chromosomal rearrangment"? (If you cannot, I can only assume you will be taking back your label of "absurd" regarding the range of mutations that exists).
I would also be interested to know if you accept that simple base-level changes could, in a way, cause position effects. Examples:
- There are master regulatory genes that have been discovered using expression-phenotype-based QTL mapping. Some of these master regulatory genes control the expression levels of several hundred other genes - it would seem to me that a subtle change in a master regulator could vastly change expression of many phenotypes in a "position effect" of sorts networked across the genome.
- Similarly, their are non-genic regulatory regions of the genome that modulate expressivity of many genes both in
cis and
trans. What of mutation of such regulatory domains? Indeed, it would seem that regional decoupling of genes from their regulatory regions is a primary cause of position effects.
You accuse me of promoting gradualism of evolution, when I am doing no such thing! I am simply suggesting various mutational modes, that though they seem "simple", or not at the karyotype-level, may actually have enormous epistatic network and/or pleiotropic consequences, resulting in saltational changes.
Dr Sasquatch asks:
2. What would you make of two (reproductively incompatible) species with the same karyotype? Would such constitute a falsification of PEH, (or perhaps an exception to PEH)?
Dr. Davison fails to respond to this point.
It may be the case, as your PEH would predict, that the above hypothetical situation does not exist. But if it did, how would you respond? Surely you realize that hypotheses must be falsifiable - would this present a falsification?
I do look forward to hearing your response, and thank you in advance for a more thought-out one than previously provided, (though I apologize if you did not understand my questions - feel free to ask me to clarify).
I feel that my explanation of a mutational spectrum with variable likelihood of resulting in saltational evolution can only strengthen the PEH!
It is so easy to believe, isn't it!
I love it so!
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