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Author Topic:   Irreducible Complexity and TalkOrigins
RickJB
Member (Idle past 5020 days)
Posts: 917
From: London, UK
Joined: 04-14-2006


Message 97 of 128 (440724)
12-14-2007 10:05 AM
Reply to: Message 96 by Suroof
12-14-2007 9:28 AM


Re: The Edge
Suroof writes:
Yes, if you have any idea as to how the irreducible core of the blood clotting system (as described in message 65) evolved in a Darwinian step-by-step model please show us.
From TalkOrigins:
Here then is an example of how such "irreducible" mutual dependencies can arise by evolution, illustrating the same process described by Muller in 1918. Miller's article goes into more detail and covers stages that I omit in this shorter account. I am simply focused here on showing the evolution of mutual dependencies, or interlocking complexity.
(A) Start with a system consisting simply of two proteins; the clot-maker and the protease. The protease is "activated" by contact with tissue proteins - as would happen when there is a break in a blood vessel. The activated protease is then able to activate the clot-maker, and the clot is formed.
(B) Now have a gene duplication for the protease. This is a reasonably common process in evolution; an entire section of the genome gets doubled; so that now there are two genes, both producing the same protease protein. There is no difference to the working of blood clotting; as all the proteins involved are the same.
(C) Now have a small modification to one of the duplicated genes. There are now two slightly different forms of the protease. Call them protease-A and protease-B. Either one would manage fine for blood clotting. In that sense, the system of three proteins is no longer irreducible; it has redundancy.
(D) Now suppose that there are mutations to protease-A which give it a capacity to activate protease-B. That is, both proteins get activated at the break in a vessel by contact with tissue proteins; but protease-B gets additional activation from the activated protease-A. This kind of additional activation can have some selective benefits, in speeding up the response of the whole system.
(E) Finally, now that protease-B is activated by protease-A, it no longer depends on activation from the tissue proteins, and further modifications can reduce this activation pathway. This makes the whole system "irreducible" again, because all three proteins are now required for clotting.
The fundamental point here is that an irreducibly complex core of three proteins can arise from a simpler system by evolutionary changes. Behe's argument depends on a strawman of evolution. Behe ignores the role of modifications to proteins, and bases his argument simply on the problem with getting a system by adding parts one by one.
Link here.
Much more interesting than "Godidit"....

This message is a reply to:
 Message 96 by Suroof, posted 12-14-2007 9:28 AM Suroof has replied

Replies to this message:
 Message 99 by Suroof, posted 12-14-2007 10:32 AM RickJB has not replied

  
RickJB
Member (Idle past 5020 days)
Posts: 917
From: London, UK
Joined: 04-14-2006


Message 103 of 128 (440747)
12-14-2007 11:36 AM
Reply to: Message 101 by Suroof
12-14-2007 10:52 AM


Re: What is your argument?
Suroof writes:
Firstly if these duplications are initially redundant but later necessary, there is no reason why they should be selected.
Gene duplication can be free from selective pressure if mutations have no deleterious effects.
Suroof writes:
Secondly gene duplication can only produce copies not complicated new steps with extremely specified features for enzyme-substrate interactions.
Gene duplication gives rise to mutation. The accumulation of mutations produce new features.

This message is a reply to:
 Message 101 by Suroof, posted 12-14-2007 10:52 AM Suroof has replied

Replies to this message:
 Message 104 by Suroof, posted 12-14-2007 11:57 AM RickJB has replied

  
RickJB
Member (Idle past 5020 days)
Posts: 917
From: London, UK
Joined: 04-14-2006


Message 107 of 128 (440772)
12-14-2007 1:45 PM
Reply to: Message 104 by Suroof
12-14-2007 11:57 AM


Re: What is your argument?
Suroof writes:
a serious model for the evolution of blood clotting would have to include such things as: a quantitative description of the starting state, including tangentially interacting systems; a description of the initial regulatory mechanisms; a quantitatively-justified proposal for a step-by-step route to the new state; a detailed plan for how regulatory mechanisms accommodated the changes; and more
Well I'm no biologist so I won't continue this line of argument. There are others here who will better answer these points.
However, I would ask you, as an ID proponent, to consider what you are arguing for:
i) ID has no model. It has no explanation for the "design" process. It makes no attempt to identify a "designer" (other than poorly veiled references to God).
ii) It makes no positive claims whatsoever. ID "research" is based entriely on nit-picking at controversial areas of evolution, seemingly unaware that problems with evolutionary theory do not automatically validate a non-existent ID model.
In short, before worrying about the "irreducible complexity" of blood clotting you should first be showing us how ID works and who is doing it.
Edited by RickJB, : No reason given.

This message is a reply to:
 Message 104 by Suroof, posted 12-14-2007 11:57 AM Suroof has not replied

Replies to this message:
 Message 108 by bluescat48, posted 12-14-2007 1:47 PM RickJB has not replied

  
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