About Rationally Speaking

Rationally Speaking is a blog maintained by Prof. Massimo Pigliucci, a philosopher at the City University of New York. The blog reflects the Enlightenment figure Marquis de Condorcet's idea of what a public intellectual (yes, we know, that's such a bad word) ought to be: someone who devotes himself to "the tracking down of prejudices in the hiding places where priests, the schools, the government, and all long-established institutions had gathered and protected them." You're welcome. Please notice that the contents of this blog can be reprinted under the standard Creative Commons license.

Monday, April 24, 2006

Reducible complexity

The main difference between creationism/intelligent design and real science is that the proponents of the former are fond to proclaim the impossibility of something (and at the same time believing in myths without a shred of evidence), while scientists are hard at work trying to figure out what is actually true by using empirical means.

A perfect example of this difference is a paper by Bridgham et al. published in the 7 April 2006 issue of Science. They studied a biological system that fits ID supporters’ definition of “irreducible complexity,” and which – accordingly – couldn’t possibly have evolved by natural means. The system in question is a classic example of “lock-and-key” at the biochemical level: an hormone receptor that binds specifically to the hormone cortisol. The question is: how could such a specific system evolve, considering that one had to have both parts (the receptor and the hormone) in place at the same time?

The elegant answer – which I predict right now will not convince any ID supporter, because their position is ideological and has nothing to do with evidence – came out of careful studies involving the reconstruction of the ancestral receptor molecule and the analysis of the kind of mutations that can change its shape.

As Darwin first pointed out, if one wishes to understand the evolution of any biological structure, one has to look as much as possible to its history, not just the current form. The latter may look impossible to explain simply because we have limited access to the intermediate forms that preceded it. So, Bridgham and colleagues used phylogenetic information on the evolution of the relevant genes to reconstruct the potential ancestor of the current receptor, and then study its biochemical characteristics in the laboratory (this is not circular reasoning: one begins by assuming evolution and making predictions: if the predictions are independently verified, this is a confirmation of the evolutionary hypothesis – standard scientific practice, no flim-flamming).

The first thing they found out about the ancestral receptor was rather surprising: not only it bound cortisol, albeit less efficiently than the current version of the molecule, but it also bound aldosterone (another hormone) and DOC (11-deoxycorticosterone). In other words, the ancestral receptor molecule had a generic biochemical ability, which is a key prediction of evolutionary theory (biological functions start out generic and become more complex and specific). How did the specific affinity for cortisol evolve?

It turns out that one needs two mutations, called L111Q and S106P, to modify the original generic receptor to a specific one. But wait! Isn’t that precisely what’s difficult to explain from a Darwinian perspective? How could two advantageous mutations happen simultaneously? And if one happened after the other, how come that the intermediate molecule persisted while waiting for the second mutation, since presumably a half-step is deleterious? (This is the molecular version of the old creationist question: what good is half an eye? The answer, by the way, is: “about half as good as a full eye”)

Bridgham et al. were able to show that in fact it makes a huge difference which of the two mutations happened first: if the L111Q appears first, then the receptor binds to nothing at all, and it becomes molecular junk, an evolutionary dead end. But if the S106P mutation happens first to the original molecule, the result is a receptor that binds only DOC and not the other two hormones. When the second mutation comes, the receptor now binds both DOC and cortisol, but not aldosterone. So one has a complete evolutionary sequence of molecular evolution, in which all the intermediates are functional, and more importantly that shows in action a basic principle of evolution: natural selection builds on previously existing materials, and in the process sometimes changes the function of those materials. No irreducible complexity needed, thank you very much.


  1. Hi,

    I'm a biology student, and you touched on something that has confused me for a while - why is the strategy of building ancestral proteins and analysing their function not circular logic? They recreate "ancestral protein" based on phylogenetic analysis, which is based on the assumption that evolution happens. If evolution didn't occur, and there was no such thing as an "ancestral protein", then any conclusions made about this ancestral protein are a moot point aren't they?
    I "believe" in evolution and I'm not a creationism/ID supporter, but if a creationist/IDer were to ask me what I just asked, I wouldn't know what to say.

  2. To the biology student:

    The question if a good one, and your confusion is very common. The reason the approach is not circular is that the ancestral protein sequences are inferred by assuming evolution, but their biochemical properties are not. The latter are studied experimentally, and they are the ones that are used to test adaptive scenarios, not the sequences. Yes, the properties do depend on the sequences, but only indirectly and in a complex fashion, which essentially decouples the two issues. I hope this helps.

  3. From my very vague understanding of "irreducible complexity" concept, isn't it just a big logical fallacy? To me, it seems like they're saying: "If evolution can show how this evolved, then it could be true. But, it can't (at the moment), therefore it is not true." Logically, If the "if" part of an implication is false, then nothing can be known about the "then" part.

  4. Continuing in jeff's vein:

    I think that what IDers think is something more like: "If evolution were capable of explaining P, then it might be true; but it isn't true, therefore it cannot explain P."

    Along comes a biologist and shows how evolution does, in fact, explain P; so the IDers shift to "If evolution were capable of explaining Q, then it might be true; but it isn't true, therefore it cannot explain Q."

    Rinse and repeat ad nauseam.

  5. I do believe things evolve; however I am curious to know how mutation plays a role in evolution. I think the main question is from people who believe in creationism is how are humans able to be different than Apes? I don't mean it in such a micro way, but rather if we all come from one gene pool how does that creature create/mutate into an ape and a human. Furthermore through geneology what about the idea of mating? Wouldn't it have been possible for lets say Apes and Humans to procreate together even though their genes have mutated slightly? Essentially according to my research we are extremely close to chimpanzees so I am just curious. No I am not ID either.

  6. Kim wrote: "... I think the main question from people who believe in creationism is how are humans able to be different than Apes?"

    I would start with the hidden assumption in there that needs to be challanged: Are we really that different from the other Apes? What is factually the same and what is different?

    This assumption is comparable to the ID idea (no pun intended) that "nature is perfectly crafted". Or my personal favorite: "nature is beautiful" (ever seen a real nature documentary? :-)

    I guess these statements usually come more from a desire than from real knowledge...


  7. I don't think creationist believe that nature is "perfectly crafted." If that were the case then events in the Bible would be disregarded as false. ie the flood, or plagues. You are misunderstanding the thoughts of creationism just as they misunderstand the theories behind evolution.

  8. Kim, there is an excellent article in Discover Magazine for April about the 2% of our genome that is defferent from that of the chimpanzee.

    But first, to split a hair if I may, humans are apes; primates lacking tails and ischial callosities. The family Hominidae (anthropoid apes) includes gorillas, onangutans, 2 species of chimp, and humans, not to mention the extinct hominids.

    Anyway, the article says that most of the genes that differ between humans and chimps are those that regulate the expression of other genes. In other words, the protein building blocks of our bodies are the same as those in chimps, but we develop slightly differently. Our faces stop growing sooner, and our brains keep growing longer. Our arms stop growing sooner, and our legs keep growing longer.

    As to possible crossbreeding, there are a diffent number of chromosomes in humans and chimps. I think one of ours used to be two, or one of theirs split. I can't remember the details. There are rumors about somebody doing the obvious experiment, but only rumors and most likely false.

    And as to your original question, mutation provides the variation that natural selection works on. If every member of a species were genetically identical, there could be no evolution. If the mutation rate is too high, the species can't be stable. If an appropriate level of mutation prevails for a long period of time, selection weeds out the monsters, and if the environment changes, some of the mutant phenotypes may do a little better.

  9. Gee

    I guess Michael Behe has no problem seeing how this system could have evolved via Natural Selection. Cool.

  10. I'm not a biologist, so I don't know the specific terminology that applies to this example, but I'll try anyway.

    In Arizona there is a kind of squirrel that lives at the south rim of the Grand Canyon, and another one that lives at the north rim. They are virtually identical, except for coloration. If I remember correctly, one is grey with a white back, and one is black with a grey back. Or something like that.

    Anyway, it has been established that both emerged from the same gene pool at some time in the far distant past. The theory is pretty straightforward: that the deepening canyon eventually separated one contiguous population into two groups, after which they evolved separately. I don't think speciation has occurred, but it's interesting anyway.

  11. Just my thought on the question "What good is half an eye anyway?" and the answer the author of the article supplied. THe author says the correct answer to this question is "Just as good as one full eye". This is incorrect as an incomplete eye (half an eye) will not ba able to function if all its components is not present. The retina is useless without the lens to focus and the muscles in the iris to control the entrace of light. What I am trying to say is that half an eye is completely useless.


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