Hi Dr. Oakley,
I am writing a research paper and came across your paper entitled, Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. I was hoping you could give me your perspective on a question that is part of my research interest.
Since a simpler mechanisms for phototransduction would theoretically work, why would evolution favor a more complicated phototransduction cascade with intermediates such as transducin and PDE? I would greatly appreciate any insight you could provide me.
The implication in the e-mail is that evolution is a force that produces sleek perfection. Expensive solutions to problems should not arise by evolution (or at least they should not be maintained), especially if the complexity is unnecessary. This is a modernist view of biology, a view that can be found in 20th Century biological research, and a view that is also common today among students, and the general public outside the field of evolutionary biology. It is a view that results from an often unstated assumption natural selection is a supremely powerful force that leads to perfection.
From this Modernist, Bauhaus perspective, it is indeed perplexing to learn that opsin initiates a complex, baroque, Rube Golddberg-like cascade to turn light energy into a nervous impulse. This cascade includes reactions from opsin->transducin->PDE->CNG; each protein signaling in one way or another to another protein down the line - and this description is even VERY simplified compared to the actual complexity!
So the question is, why would evolution "favor this complicated phototransduction cascade", when all that seems to matter is that opsin signal directly to the CNG ion channel protein to cause the nervous impulse.
The most direct answer is that evolution is not an Intelligent Designer, rather it is a bricoleur, a tinkerer. Evolution acts upon what is available, and things that are useful are kept. In the case of the phototransduction cascade, evolution co-opted existing components: an existing GPCR cascade gained light sensitivity. We know this because the components of phototransduction pre-date opsin (e.g. here). Phototransduction was not invented from scratch, in the most efficient way possible. Instead, it was cobbled together using available parts.
This can be conceived as an example of a phylogenetic or historical constraint. In other words, history matters. All living things and all components of living things share a common history. Because of this, and because of the interdependence of components of living things, it is usually not easy to completely re-invent something. The number of shared genes in all animals (for example) clearly illustrates that history matters. Components are used and re-used, not invented anew.
This answers the proximate question, of why phototransduction is so complex. But doesn't address the question of why all GPCR cascades are so complex. I don't know the answer to this, but perhaps the complexity allows for flexibility. In fact, GPCR cascades are supremely flexible, and underlie signaling from outside to inside cells for many processes in animals, including vision and other senses, hormone signaling, metabolism, development, reproduction, etc, etc.
Interestingly, this question showed me yet another new perspective on the flawed argument for Intelligent Design. ID proponents suggest that when we see something outlandishly complex, then it must have been designed by an intelligent agent. However, as this question points out, extravagant complexity is not a sign of intelligence. Why use 50 components when 2 will suffice? Elegant simplicity is far more intelligent than excessive complexity. Again, evolutionary biology provides a logical and plausible explanation for the biological processes that we are coming to understand.
7 comments:
Outlandish complexity = intelligent agency is not what ID proponents argue. Repeatedly, William Dembski and Stephen Meyer have argued that more than complexity is necessary to make a design inference; specification is also necessary. Specification demonstrates functional significance and therefore a much smaller probability of occurence. For example, the combination of characters and spaces "tno awyobeqz ucpemony" is complex since it is a highly improbable combination of letters and spaces, but it has no function. Could it have come about randomly? Sure. However, the phrase "John rode his bike" is both complex and specified; therefore, Dembski argues, that since the probability of those characters and spaces coming together at random to produce complex, functional information is so low that an inference to design can be made. Additionally, in "Signature in the Cell," Stephen Meyer argues that since intelligent agency is casually adequate to produce complex, specified information and the only known cause of such information is intelligent agency, one can claim intelligent agency as the best explanation for that information.
Interestingly enough, complex, specified information is found in DNA. Now, whether or not some form of evolution (obviously not the Darwinian form)played a part in the development of the eye remains to be seen; however, ID theorists argue convincingly that the cause of the complex and specified information within DNA is not the result of a random, undirected process.
melech - Yes, I think you are right that the ID conception of complexity has more to do with functionality than with the # of parts. ('Specification' sounds like design though, and I don't see how that can be inferred without just assuming it, so I prefer to think about the functionality/usefulness/adaptedness. These can be defined).
I do disagree about other things though. It does not, in fact, remain to be seen that Darwinian evolution caused eyes. This hypothesis has been tested in numerous ways, and has been supported. I've written about many of the tests and supporting evidence on this blog.
Yes, it's true that complex, functional information (in DNA) cannot be the result of a random, undirected process. It in fact takes a non-random process, like natural selection. We didn't need ID theorists to realize that random undirected processes cannot produce functional complexity - no one claims that, it takes a directed process like natural selection.
I really appreciate the kind response. I dont get many kind responses from evolution proponents.
Like Dembski and Meyer, I dont contest the fact that random mutation in DNA can cause novel changes. The contention arises with the claim that the specified, complex information contained within cells originated from a random directionless process.
Whenever I used the term "specified information" I actually mean "functional information". Dembski equates the two since the terms mean the same thing in the context Dembski uses. Additionally, Meyer argues that one way specification can be identified is when one knows it from an independent field of experience. I can identify that a pattern is specified information even when it is in different forms because I know the pattern from an independent field of experience. Functional protein molecules qualify for the design inference because their sequence is the same as the independent pattern required for functionality. Complex, specified information coupled with the extremely low probability of such a sequence randomly obtaining, these sequences finally meet the requirements of Dembski's explanatory filter for inferring design.
As far as the development of the eye is concerned, I'm aware of the arguments concerning co-option of subsystems. I meant that while a (non-darwinian)theory within ID which accounts for the evolution of the eye does not yet exist, one potentially could exist. I'm sorry. I should have been more clear.
I've heard a couple times (only from proponents of evolution)that natural selection is a directed process but no one has ever explained to me what part is directed. What about natural selection is directed?
Melech asked
I've heard a couple times (only from proponents of evolution)that natural selection is a directed process but no one has ever explained to me what part is directed. What about natural selection is directed?
In a population of replicators (critters) there is always phenotypic variation generated by mutations and several sorts of genetic cross-talk among individuals (horizontal gene transfer and sexual mating, to name two). Some of the variants in the population are more reproductively successful in the population's environment than others -- their particular heritable traits give them some advantage in the competition for mates, space, and resources, and their offspring are similarly more reproductively successful. Such lineages come to dominate the population at the expense of lineages that are less reproductively successful.
That difference in the reproductive success of lineages which leads (over generations) to a change in the composition of the population in a given selective environment is what 'directs' the process. It's not direction from an external source except insofar as the selective environment can be considered an external source, and it occurs as an inevitable consequence of the operation of the mechanisms themselves -- variation generation and differential reproductive success.
And for the kibitzers, yes I know that's simplified and ignores things like genetic drift. Comments are not dissertations.
RBH - Well said. I've been meaning to write something like that, but hadn't found the time lately.
Very nice post on the tinkering aspects of evolution.
Regarding the question of cascade complexity (in the sense of having many intermediate steps): I guess one reason for this is that this is a biological amplifier: at each step an effector can activate several downstream targets, each of which can activate several downstream targets, etc.
Nice post on evolution! Very thoughtful and helpful
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