In a message dated 10/1/2000 11:37:34 PM Pacific Daylight Time, DNAunion
writes:
> >FMAJ: Robison has shown a potential pathway to an IC system. Robison shows
> a natural pathway to an IC system
> http://www.talkorigins.org/faqs/behe/review.html
> Behe responded to the article but seems to have missed the point.
>
> DNAunion: How did Behe miss the point? Surely Behe's objection to
> Robinson claiming the TCA cycle was IC, then showing it wasn't, is valid.
You seem to be missing the point as well. Did you read the article in which
Robison shows a pathway to an IC system.
As Behe points out, Behe never said the TCA cycle was IC. This comes awfully
close to a straw man argument (making a claim the opponent doesn't with the
> intent of showing the claim to be false and thereby supposedly refuting the
> opponent's position). I have seen many instances in which anti-IDists
> "move the goal posts" to get something supposedly labeled as IC with the
> sole intent of then showing that it could arise naturally, thereby (again,
> supposedly) refuting the IC concept. This appears to be what Robinson did.
>
Did he now? And why do you not focus on Robison's argument that showed a
natural pathway rather than attack a strawman yourself? But that Robison
considers the TCA IC based on his interpretation of Behe's definitions hardly
makes it a strawman. Behe seems to be moving the goalposts when he gets to
reject or accept ICness.
> I also agree with Behe that Robinson did not reduce the mouse trap by
> substituting a wood floor for the base - the same number of functional
> pieces were present as where the same number of functions.
>
Still missing the point.
> I also agree with Behe (though I think he may have not been clear in his
> book) that his argument was not that pseudogenes themselves could not arise
> naturally, but that the mechanisms needed to produce them (the mechanisms
> of normal cellular information flow that malfunction to produce
> pseudogenes) could not have.
>
Still missing the point.Read the part about cascades. And pseudogenes
http://med-humgen14.bu.edu/ota/publication/CTML95/CTML951.html
http://www-polisci.mit.edu/bostonreview/br22.1/futuyma.html
http://www.world-of-dawkins.com/box/published.htm
> >FMAJ: A classification of possible routes of Darwinian evolution. Richard
> H.
> Thornhill1 and David W. Ussery. Published in The Journal of Theoretical
> Biology, 203: 111-116, 2000. "Possible routes of Darwinian evolution can
> be classified into four fundamental categories, as outlined below."
>
> DNAunion: Mike Gene posted about this article at ARN, and David Ussery even
> posted there in response to Mike's post. Perhap's Mike would fill us in
> (keeping in mind that it MIGHT not be proper to quote David Ussery here -
> though quoting others' work does seem to occur quite frequently here).
>
I'd love to see some comments of Robison' s cascade and the Thornhill paper.
More on Ussery: http://www.cbs.dtu.dk/dave/Behe.html
http://www.cbs.dtu.dk/dave/JTB.html
http://www.cbs.dtu.dk/dave/Behe1.html has the link to the ARN forum
> >DNAunion: Anyway, could you provide more material as to how Behe's concept
> of IC has been refuted?
>
> >FMAJ: What has been shown is that 1) direct routes exist 2) indirect
> routes may
> exist. This means that ICness itself is not a reliable indicator of design.
>
> DNAunion: Again, what is the exact natural "direct route" of generating IC
> and what is the supporting evidence?
I just showed you two references. What is the supporting evidence? Well
that's were science will have to do some work. But my point is that ICness is
not a reliable detector of design anymore. Does this mean that science will
not have to explain IC systems ? Of course not. Several good pathways have
been shown.
Can evidence be found to support that these pathways actually happened? That
will depend on the system. Molecular 'machines' do not fossilize. Does this
mean that we perhaps will never find the data to support a darwinian origin?
Perhaps. Does this mean that we therefore should infer design? Of course not.
Robison:
Starting pathway.
X<---X* has been omitted from diagram. This is hypothesized to be either
spontaneous or catalyzed by X*. (Both cases are known to
exist). A stimulus triggers the conversion of X to X*, and X*
autocatalytically drives this conversion also. X* then acts on a target.
Post gene duplication.
This is a completely symmetric system. (The diagram is not, but could be
rearranged into one.) This arrangement is neutral; the species
has gained no advantage. On the other hand, duplications such as this are
a common event.
Mutation eliminates X*'s ability to interact with target.
The duplicate is now labeled Y/Y* for clarity. Again, this genotype is
neutral; it is neither beneficial nor detrimental. Once a duplication
occurs, mutations partially inactivating one copy will be common.
(Mutations completely inactivating one copy will also be common,
restoring the system to its initial state.)
Multiple mutational outcomes are now possible:
X is inactivated by mutation.
System returns to start.
Y* catalytic activity for X->X* and Y->Y* conversions is lost.
System is now dependent on X and Y. (Stimulus alone is not
sufficient for useful activation.) It has become "irreducibly complex."
Y's ability to respond to stimulus is lost.
System is now dependent on X and Y. It has become "irreducibly
complex."
So, duplication plus a loss of function, plus one of two different
loss-of-function mutations can convert a single step pathway into a two
step cascade. The initial steps are neutral, neither advantageous nor
disadvantageous. Such neutral mutations occur regularly. The final
step locks in the cascade. It is potentially advantageous, because
multiple levels of cascade give opportunities for both control (probably
a long-term advantage) and for amplification. (One X* can activate many
Y's, increasing an initial signal.)
It should be obvious that either the target or stimulus could be another
such pathway, and so this mechanism could expand the number
of layers in a cascade. And, both outcomes retained a degree of
autocatalysis, again leaving opportunity for more cycles of layer
expansion. So much for "irreducible complexity".
This is, of course, a model. A model should make predictions, and this
model does. If a pathway evolved by such a manner, then
consecutive steps in the pathway should be catalyzed by homologous
proteins (a characteristic of both the blood coagulation and
complement cascades, two examples given by Behe). If the proteins are
encoded by adjacent genes (tandem duplication) or one gene
shows the hallmarks of reverse transcription (no introns and a poly-A
tail in the genomic sequence), all the better. We would also expect
to find systems in nature with fewer or greater levels of cascading.
Here is another one
Orr says it best in his perceptive review:
"Behe's colossal mistake is that, in rejecting these possibilities, he
concludes that no Darwinian solution remains. But
one does. It is this: An irreducibly complex system can be built
gradually by adding parts that, while initially just
advantageous, become-because of later changes-essential. The logic is
very simple. Some part (A) initially does
some job (and not very well, perhaps). Another part (B) later gets added
because it helps A. This new part isn't
essential, it merely improves things. But later on, A (or something
else) may change in such a way that B now
becomes indispensable. This process continues as further parts get
folded into the system. And at the end of the day,
many parts may all be required."
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