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.
>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.
>>>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. The two-spine mutation you mentioned, for
example, I don't see that succeeding. 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.
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'. 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.
--Cliff Lundberg ~ San Francisco ~ 415-648-0208 ~ cliff@cab.com
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