Like many scientists, I make use of Web of Science and PubMed to alert me when papers in my field of research are published or when one of my articles is cited. The latter may sound vain, but in fact it is helpful because one’s papers sometimes are cited in unexpected ways that would probably not be discovered by one’s routine literature searches.
This post is about an intriguing example of a connection that I never would have drawn myself and which I probably would not have seen in the literature had I not been alerted that some of my articles on genome size and non-coding DNA had been cited. Specifically, this involves two recent papers on what I would have assumed was a totally unrelated topic: sleep.
I am sure that everyone reading this blog is familiar with the importance of sleep in a physiological sense — if you don’t sleep for a large portion (~1/3!) of every day, both your mind and body suffer. However, in an evolutionary sense, why we sleep remains something of a puzzle. As Savage and West (2007) put it, “Sleep is one of the most noticeable and widespread phenomena occurring in multicellular animals. Nevertheless, no consensus for a theory of its origins has emerged.”
So what does this have to do with non-coding DNA?
In the first paper mentioned above, Savage and West (2007) put forth a framework for studying the function of sleep that relates to cellular damage repair and brain reorganization. This includes linkages with metabolism, body size, and cell size, the latter of which is related to genome size, and thus to the quantity of non-coding DNA. Moreover, the amount of DNA per genome may be related to the genome’s susceptibility to mutational damage (though this remains to be established, and one could come up with a priori arguments for why the relationship might be positive or negative). So, in this case, the amount of non-coding DNA may relate to one or more of the proposed functions of sleep, and thus be relevant to an adaptive interpretation of the question. Interesting stuff.
The second paper, by Rial et al. (2007), takes a rather different approach to the question. They argue that sleep per se is not really necessary — rest would suffice. These authors invoke non-coding DNA not as a possible factor of interest in explanations of sleep, but as an analogy. In particular, Rial and colleagues lament the fact that sleep is almost always approached from an adaptive standpoint because it is relatively complex. “However,” they write, “complexity is not by itself ï¬rm proof of adaptation. A well known, complex, but seemingly useless structure, could be invoked as a metaphor for the uselessness of many sleep signs.” That complex, (possibly) largely functionless feature is, you guessed it, non-coding DNA. Sleep, under their interpretation, may be more like non-coding DNA than like the eye, in that it is not the product of adaptation but rather reflects a byproduct of other processes. In addition, whereas some non-coding DNA takes on a secondary function, so may have some components of sleep.
I am not qualified to comment on the scientific merit of either hypothesis, so I will not say any more about their specific arguments. I am, however, pleasantly surprised to see non-coding DNA making an appearance, both mechanistically and conceptually, in discussions of what I would have thought was an unrelated subject of inquiry. It just goes to show the interconnectedness of science, and the importance of reading outside the bounds of one’s own specialized field.
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References
Rial, R.B., M. del Carmen Nicolau, A. Gamundi, M. Akaarir, S. Aparicio, C. Garau, S. Tejada, C. Roca, L. Gene, D. Moranta, and S. Esteban. 2007. The trivial function of sleep. Sleep Medicine Reviews, in press.
Savage, V.M. and G.B. West. 2007. A quantitative, theoretical framework for understanding mammalian sleep. Proceedings of the National Academy of Sciences of the USA 104: 1051-1056.