Irreducible Complexity as an Evolutionary Prediction

Post of the Month: September 2006

by

Subject:    Re: An early IC prediction
Date:       21 September 2006
Message-ID: 1158845586.657524.69690@k70g2000cwa.googlegroups.com

Soren K wrote:
> Hi
>
> I remember once finding a mention of a biologist in the first half of
> the last century who predicted that evolution would sometimes make
> systems that seemed impossible to develop stepwise. It was mentioned as
> a counterpoint to Behes idea of irreducible complexity, which is
> basically the same idea, but the other way around.
>
> Do any of you know more about this. I need a citation or at least the
> name of the biologist for a debate I'm having elsewhere, but I cannot
> find it right now.

The name you might be looking for is Herman Muller.

Here's the detail, reworked from a post I wrote at an on-line web forum.

Herman Muller, in 1918, indicated that an expected result of evolutionary processes was the development of what he called "interlocking complexity". Muller was one of the great geneticists of the twentieth century. He went on to win a Nobel in 1946 for work in mutations.
<http://nobelprize.org/nobel_prizes/lists/1946.html>

Muller's definition of "interlocking complexity" is exactly the same as the definition of "irreducible complexity" -- a system of mutually independent parts that requires all those parts to be present for the system to work. However, Muller's claim is that this is an EXPECTED result of evolution. Behe took the same definition, and claimed it was IMPOSSIBLE as a result of evolution.

The reason for the difference is basically that Muller was using evolution; and Behe was using a weird strawman of his own devising. Behe describes evolution as working by the gradual addition of parts, one by one. Muller, however, describes evolution as working by gradual modifications of parts. Muller's description is the more accurate. New proteins don't get added to systems particularly often; the vast majority of evolution is small modifications to proteins, to alter their amino acid sequence and hence their chemistry. Behe neglects this entirely; and hence omits the vast majority of evolutionary change.

The paper is "Genetic Variablity, Twin Hybrids and Constant Hybrids, in a Case of Balanced Lethal Factors", by Hermann J Muller, in Genetics, Vol 3, No 5, Sept 1918, pp 422-499. You can read a scan of the paper online at <http://www.genetics.org/content/vol3/issue5/index.shtml>.

Here is a relevant extract, from pages 463-464 of the article:

... Most present day animals are the result of a long process of evolution, in which at least thousands of mutations must have taken place. Each new mutant in turn must have derived its survival value from the effect which it produced upon the "reaction system" that had been brought into being by the many previously formed factors in cooperation; thus a complicated machine was gradually built up whose effective working was dependent upon the interlocking action of very numerous elementary parts or factors, and many of the characters are factors which, when new, where originally merely an asset finally become necessary because other necessary characters and factors had subsequently become changed so as to be dependent on the former. It must result, in consequence, that a dropping out of, or even a slight change in any one of these parts is very likely to disturb fatally the whole machinery; ...

The evolution of the blood clotting system can be used as an example to show how this works. It's pertinent, as Behe gives this as an example of IC. A more complete account of how blood clotting cascades can arise is given in The Evolution of Vertebrate Blood Clotting, by Ken Miller, online at <http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html>.

I'll paraphrase his section "Introducing Complexity", which gives a simple example of just the process Muller described in 1918.

First, the core of blood clotting is a "clot-maker" protein, which has a kind of "sticky" section in the middle of the protein, and this is normally covered by smaller chains of amino acids. Another protein (a "protease") can "activate" the clotting process by clipping off the covering chains of the clot-maker, exposing the central section. The clot-maker proteins then bind together into a solid mass that makes up the clot.

However, the full process in humans, or any vertebrates, is much more intricate, involving a whole chain of proteins, each of which acts to "activate" the next in a whole chain of activations, ending up with activation of the clot-maker. The claim of irreducible complexity is basically the claim that removal of any protein from the chain would make the whole process fail.

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.

Miller's article goes into a lot more detail, describing how the initial two protein system can form, and giving examples of known organisms with functional blood clotting systems that do indeed represent intermediate stages in this kind of development.

Muller did not know the details of blood clotting cascades, but he had already in 1918 correctly anticipated the processes by which a system composed of many mutually interdependent parts would be expected to arise by evolution.

Cheers -- Chris Ho-Stuart

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