There is a discussion on the internet about Junk DNA, that includes a discussion at Sandwalk (Larry Moran’s blog) … I made a comment there about genome size that was responded to by T.R. Gregory. I started to write my response in Larry’s Little Box, but realized that it would not fit. So it is here:


Imagine a gene family distributed among all the species in a given taxon. There are several alleles per gene. The gene codes for an enzyme that plays a role in determining cell size. Different combinations of genes/alleles exist to cause cell size to vary such that each species has a typical range of cell size, and the species – distributed among various genera – vary at a larger scale in cell size. Metabolic activity relates to cell size. The species with the smallest cells also have adaptations that are matched by high cellular metabolic rates, the species with largest cells have adaptations that are matched by lower cellular metabolic rates (the smaller celled species fly, the larger celled species hibernate, etc.) such that there is a general correspondence between variation among the species (and clinally within some or all of the species) between cellular metabolism and other ecological or life history adaptations.

A scientist, Dr. P. Gloss, proposes that selection has acted on these species in different ways, such that the genes in this gene family have been selected for (duplication has a fitness effect) and against (mutations converting genes to pseudogenes has a fitness effect), and the alleles selected as well, and that there is co-evolution between the evolutionary dynamics of this gene family and other genetic systems related to the various adaptations under consideration.

This is not a bad story, and would probably enter into the Annals of Adaptive Explanations as a textbook case.

Subsequently, it is found that the common ancestors of the smallest-celled genera and the largest-celled genera were all pretty similar to each other (as far as one can tell from the fossils), but that the cell size back in those days had a similar distribution to what we see in the modern, living forms. In other words, cell size did not seem to be incorporated into an adaptive syndrome X millions of years ago, even though it is now.

Now the story passes into the Annals of Anti-Adaptationism, as Gouldian exaptationists and anti-adaptationists and Neutral Theorists revel in the fact that the cell size distribution arose independently of (prior to) later adaptations. Perhaps cell size is a constraint, but it is not an adaptation. The evolutionary history of this family of genes can now be seen as non-adaptional, drift like.

However, a diligent field worker discovers that within a given taxon, there is a strong correlation between the distribution of the cell-size alleles, the actual cell size (as expected), and clinal variation in adaptations related to cellular metabolism, in several of the species under discussion. She shows through field experimentation that individuals with the inappropriate cell size, when transferred between ecological settings, have lower fitness. She shows through a combination of laboratory work, simulation modeling, extensive field data, and the field experiments that she can predict fitness from the genome with respect to these systems. Indeed, there are a handful of examples of species or subspecies that are seen to have a reversed evolutionary trend from their close relatives (a large-celled species in a small-celled genus, and visa versa) wherein the biogeographical and ecological history of these taxa show that those “reversals” would likely have arisen from selection.

The story moves back into the Annals of Adaptive Explanations at one level, but remains in the Annals of Anti-Adaptationism in other ways.

Now consider the above outlined (imaginary) story in comparison to the genome size story with birds. Birds and bats require a high measure of metabolic efficiency, and thus, small cells might be selected for in these animals. They also have smaller than expected genomes, which in fact gives them these small cells. On first blush, there seems to be an adaptive story here. But then it is discovered that the ancestors of birds (though I think we don’t know this for bats) is one of a group of non-flying, and thus presumably not requiring a high degree of cellular metabolic efficiency, creatures. Is it the case that small cell size caused by small genome size is no longer an adpatation?

Maybe. But our diligent field biologist comes back on the scene. Through manipulation of the genome, she carries out experiments to test the relationship between cell size and genome size and fitness in birds and bats. By enlargement of the genome of experimental groups of birds and bats, she shows that they have significantly reduced fitness. She also finds out that birds that do not fly have larger genomes than birds that do fly, and that there are nine or ten other tetrapods that do not fly but still require small cells for some reason, and they have small genomes, and so on.

In the mean time, a paleontologist working on the ancestral birds and their relatives discovers evidence to deduce a plausible hypothesis that this particular group of extinct critters required a high cellular metabolic rate. This could explain the observation that this group has small cells. It turns out that birds evolved from a form that had, though natural selection, ended up with small cells. Another paleomammalogist discovers that he non-flying ancestor of bats also had small cells, and were members of a broader taxon also with small cells, and there was some ecological reason for this metabolic syndrome. So, in this hypothetical case, both birds and bats emerged from groups that had small cells for adaptive reasons, and incorporated this trait in a different, novel adaptive syndrome (flight).

There are two points that emerge from this twisted story of changing perspectives. First, how do we treat classic genetic systems (a gene codes for a protein that has a function, and this function varies across genetic forms in a way that affects fitness) and non-classic genetic systems (in this case genome size) when we are talking about adaptations? In the discussion we are seeing right now on the internet, there is a distinction being implied. It may be a proper distinction in some cases, but possibly not in others. Is the fact (assuming it is true) that sometimes genome size fits an adaptive story and sometimes it does not …. even when it is the same story but with different degrees of understanding the details … suggestive of the possibility that the differences are actually semantic? Or at least, that our rhetorical framework for adaptation is inadequate?

The second point is in reference not to classic gene stories vs. other heritable features, but to adaptation itself. The first time I read of the concept of “exaptation” (Gould and Vrba) I thought that every adaptation must be an exaptation, or most of them anyway. I thought that the only real adaptations … adaptations that do not incorporate prior function in a novel way … must be either created by some sort of god, or must date to the very origins of life. I still think this. This is why you don’t hear me using the terms “aptation” and “exaptation” as Gould and Vrba suggested. I would say that most adaptations have historical contexts that disallow clean separation of the historical process of the adaptation (its emergence through selection) from the broader context. Life is complex. The history of life is more complex. Adaptations are not things. They are processes.

Comments

  1. #1 TR Gregory
    January 18, 2008

    This is indeed the nature of the issue. It is also why I don’t ascribe to either the adaptationist or neutralist camp (if such there truly be) when it comes to such a complicated topic. We are doing work on quite a number of the questions you cited, so stay tuned.

  2. #2 Greg Laden
    January 18, 2008

    I have always thought that both the logic and empirical support for adaptationist approaches and neutral approaches were very good but oversimplifid. This is an issue I have thought a great deal about, and I have concluded that both approaches can be accommodated, but neither is very powerful as a model for evolution.

  3. #3 Larry Moran
    January 18, 2008

    I’m not sure if I follow the logic here. Are you saying that there might be pressure to make smaller cells but the only easy way to do that is to get rid of junk DNA?

    How, exactly, would this work? Let’s say you have some variation in the population where there are some individuals with 1% less DNA in their genomes? Would those individuals have a significant enough selective advantage to ensure fixation of the smaller genome?

    Does it follow from your scenario that the bloating of the genome in our ancestors had no detrimenatl effect even though it might have led to larger cells and slower metabolic activity? If so, doesn’t that mean that the junk really is junk in most species?

    I still don’t see how your hypothesis leads you to claim that junk DNA is a myth.

  4. #4 Greg Laden
    January 18, 2008

    I’m not sure if I follow the logic here. Are you saying that there might be pressure to make smaller cells but the only easy way to do that is to get rid of junk DNA?

    No, I am not saying that.

    I still don’t see how your hypothesis leads you to claim that junk DNA is a myth.

    I am not making that connection, nor am I claiming that “junk DNA is a myth.”

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