Re: Spliceosomal introns


"Perplexed in Peoria" <jimmenegay@xxxxxxxxxxxxx> wrote in message
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"g" <gillawton@xxxxxxxxxxxxx> wrote in message
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The MAIN questions I have surround not whether germline cells are
communicated with by somatic cells (adjacent, neuronal...?) or by way of
enzymes in the blood, or by way of lymphatic or other routes...
They HAVE to be triggered to degress, or the kitten eye taping experiment
would not turn out as it does. Also, if the germline cells were not
communicated with in cave creatures and burrowing creatures that live in
dark environments, those creatures would not end up blind.

Sure they would, for the same reason that fruit eating mammals ended
up without the ability to synthesize vitamin C.

So are you saying that the reason fruit eating mammals began to repress
their genes coding for proteins to make ascorbic acid is because those genes
got no stimulus to act? That would be a "spring loaded off" position,
awaiting a pH level above a triggering point to turn on, and not getting any
action for several generations due to the pH level being kept high by fruit
diet for several generations.

But then, again, mathematically there would several scenarios to hypothesize
and rule out by a variety of experimental scenarios.

Perhaps a suppressor gene (or gene splice switch) would stay in the "on"
status, awaiting a high pH and, not getting it for several generations,
"lock" in the "on position" to suppress.

If all the different trial hypotheses were to be calculated, the simplest
scenarios would be those involving a single gene with alternative splicing
to switch into "on" (make some ascorbic acid) and otherwise remain "off"
until the appropriate bio-chemical trigger condition switches to the "off"
(don't make any ascorbic acid) position.

If there is, on the other hand, a gene that stays on, but is suppressed by
another gene until pH turns it off, this would require more trial hypotheses
to check out, and the suppressor gene would have to be found.

The result of any of the various logic switching scenarios would be six of
one and half dozen of the other, in an animal that does have ascorbic acid
fabrication capacity. Whether it takes only one gene to code for the
fabrication AND to regulate when to make and when not to make, or TWO genes,
one coding for making and normally on, with another to regulated when and
when not to... that would be a more complex logic circuit.

Hmmmmmm. Am thinking how each hypothesis would be tested.

I wonder if a good first step would be to find a proper laboratory animal
that can make its own ascorbic acid and overdose it with ascorbic acid for
thirty or forty generations.

What else? Maybe we could try to create some laboratory mouse chimeras,
replacing their (pseudo-gene???) that does not make ascorbic acid with a
gene from some species (animal or plant) that can make its own ascorbic
acid. Then, if that does not work, we would know to look for a suppressor
gene to knock out.

It would be a process of elimination by mixing and matching.

But how wide a spectrum of DNA would we have to sort through to find a
suppressor gene, if it exists?
Are suppressor genes and the genes they suppress normally found proximate to
one another?

But wait... it seems the first thing we would need to do is examine the
human pseudo gene (or whatever it is called) which does not code for a
protein that leads to the making of ascorbic acid and examine the gene found
in animals that do make their own ascorbic acid. Then we could make a
chimera that has the
"make ascorbic acid gene" in its chromosome package from one parent, and not
the other, and see if it is recessive.





.

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