From: Cliff Lundberg <cliff@cab.com>
>Richard Wein wrote:
>
>>>>>>You're still evading my question of whether we ever see heritable
>>>>>>Siamese-twinning in humans. If not, then your claim that we see this
>>>>>>mechanism in humans is false.
>>>
>>>This is a triviality to the theory in question, something I would happily
>>>scratch from the article if I were convinced you were right about this
rare
>>>phenomenon. The big point is simply that Siamese-twinning is a mechanism
>>>for generating morphological complexity, a mechanism that we can
>>understand.
>>
>>I'm not clear what you mean by this.
>
>You don't think a set of Siamese twins is more complex than a lone
>normal individual? I suppose in some informational/genetic sense they
>aren't; I suppose in that sense a two-legged organism is no more complex
>than a one-legged one. But I'm talking about morphology, and I'm being
>specific about my definition of 'complexity' for purposes of communicating
>this model: number of parts.
I wasn't referring to your statement about complexity; I was referring to
your statement about heritability, as the following questions should have
made clear.
>>Are you withdrawing your claim that the mechanism underlying your
>>theory (heritable Siamese-twinning) is observed in humans?
>>
>>Or are you saying that heritability of Siamese-Twinning is unimportant to
>>your theory?
>
>Heritability of S-t is necessary. What is not important is whether or not
>there are instances of non-heritable S-t. If there are such, and I'm sure
>there are, this has no particular connection to humans, who are just
>another metazoan species for my purposes here.
So are you withdrawing your claim that the mechanism underlying your theory
(heritable Siamese-twinning) is observed in humans?
And since you agree that heritability of Siamese twinning is necessary,
*how* do you think it's inherited? I mentioned the possibility of
duplication of the whole genome, but you didn't seem to like that. What
mechanism do you propose?
>>>>And I come back to the point that I made earlier. Partial Siamese
twinning
>>>>shows that a simple chance disruption during development can result in
>>>>functional duplicate limbs and organs, even in an organism as complex as
a
>>>>human. If this can happen when the disruption is by chance, why can't it
>>>>also happen when the disruption is due to a simple mutation?
>>>
>>>Duplicate limbs and groups of organs, fine. Gradual serial accretion of
new
>>>segments within sets of homologs, no way.
>>
>>This seems to be a substantial concession, so let me make sure I
understand
>>you. Do you now agree that limbs and organs may be duplicated as the
result
>>of a simple mutation, i.e. not necessarily due to reactivation of an
>>atavistic gene?
>>
>>If you now agree with this, then much of our discussion, such as
polydactyly
>>in humans, loses its relevance. So I'll wait for your reply before
>>continuing.
>
>When I said "duplicate limbs and groups of organs, fine", I was only
>agreeing that a Siamese twin may consist of part of the complete
>organism, and that this part may include some limbs, some organs,
>some whatever. But this is too crude a mechanism to insert useful
>additional segments or organs into an organism, too crude to usefully
>elaborate morphology.
Hang on. You just said that a Siamese twin may include some organs. Then you
said that this mechanism is too crude to insert useful organs. What does
this mean? Are you saying that a Siamese twin can include a useless organ
but not a useful one? But we see Siamese twins with fully functional
duplicate organs.
>The two-spine mutation you mentioned, for
>example, I don't see that succeeding.
Why not? If this deformity can result from a simple environmental variation,
such as the presence of an area of low oxygen content, then why is it so
hard to believe that a similar deformity could result from a mutation?
>I don't see how a Siamese twin
>can be so fortuitously reduced and positioned so as to comprise one
>new functional item within a set of homologs in its sibling. I don't
>think that a hexadactyl individual could result from having 4 identical
>twin siblings, each reduced to one digit and positioned correctly. It's not
>impossible, but it's astronomically unlikely.
You've missed my point. I'm not saying that hexydactyly results from Siamese
twinning. Please re-read my point above ("And I come back to the point that
I made earlier...").
>My model relies on regulatory genes to shape the organism from a
>progenitor which is informationally simple but complex in terms of
>number of parts. The information for the symmetrical progenitor
>with many parts remains, but regulatory genes limit and distort its
>expression during development. Perhaps there is room for agreement
>there, perhaps these are your 'control genes'.
Yes, "regulatory genes" seems to be the more common term, though I've also
seen "control genes".
>But in my model these
>genes do not create brand-new segments, they do not elaborate sets
>of homologous structures with new members. Atavistic elaborations
>may occur which have more segments, but this is only expression
>of normally suppressed structures which were there from the start.
Yes, I understand that that is what your model says.
Richard Wein (Tich)
This archive was generated by hypermail 2b29 : Tue Jun 20 2000 - 17:52:35 EDT