Finally, I will finish this blog post, which I started months ago! I've been sooo busy with various things, including writing a paper (now in submission) and finishing off work for a handful of side projects, that my blog has become seriously neglected. However, now I have a (relatively) spare afternoon that I can devote to a bit of reading and blogging.
The paper that I'm hastily refreshing my memory about is "Non-adaptive origins of interactome complexity". However, I'm not going to blog too much about it, because PsiWaveFunction has written a very detailed piece, that I highly recommend checking out. However, I'm very interested in this paper, so I can't resist blogging just a little bit about it!
In the paper, Ariel Fernández and Michael Lynch consider the effect of population sizes on evolution of complexity, as measured by the number of protein-protein interactions. Multicellular eukaryotes have small popualtion sizes as compared to microbes, which leaves them vulnerable to the phenomenon of genetic drift, where changes get fixed in the population because they fail to get filtered out by efficient selection. These changes can sometimes be mildly deleterious. The type of deleterious mutations considered in this study are those that increase the area of the protein in contact with water (the protein-water interface or PWI), and so reduce the stability of the protein in solution.
The authors find a correlation between drift and protein structural integrity, and suggest "that the emergence of unfavourable PWIs promotes the secondary recruitment of novel protein–protein associations that restore structural stability by reducing PWI". So essentially, proteins are recruited into multi-subunit complexes not to explore some new functional space as is commonly thought, but rather to stabilise decrepit proteins that have evolved through drift, itself caused by small population sizes.
Like I've blogged about previously, evolution does not always lead to the optimal solution. Just as long as a system is good enough to work, that's fine. And if that means employing some elaborate hacky, complex solution, that's not a problem (just as long as you can handle a flabby genome).
I like coming up with silly analogies, and in this case it's complexity as a crutch. Eukaryotic proteins are careless and clumsy, They end up lame, and although they can hobble around enough to get by, its easier with molecular crutches. But the big question is what is the order of events? Was the crutch being used before or after the protein became lame. Lukeš et al. argue that eukaryotic proteins were already messing about with crutches even before they needed them. This is so-called presupression or constructive neutral evolution (CNE).
Presupression is a ratchet-like process, which Lukeš et al explain as follows:
"A biochemical reaction under selection is catalyzed by a cellular component A (nucleic acid or protein) that fortuitously interacts with component B either directly, by binding, or indirectly, through the products of B’s own selected activity... The interaction, though not under selection, permits (suppresses) mutations in A that would otherwise inactivate it. Under these conditions, mutations will unavoidably occur, making A dependent on B."
But actually, both these models are not mutually exclusive. Whether in some cases complexity is a crutch that overcomes the limp of an already hobbling protein, or whether it is a fortuitous accessory which eventually becomes depended upon, we are beginning to understand that increasing complexity is probably largely a non-adaptive phenomenon, and not neccessarily the function builder that was previously thought.
And now I'll direct you over to the fabulous Sceptic Wonder blog by PsiWaveFunction, who's done an astounding job covering the Fernández and Lynch paper.
Also, watch this blog space for further discussion of the Lukeš et al paper, specifically their description of ribosome evolution under CNE.
Fernández A, & Lynch M (2011). Non-adaptive origins of interactome complexity. Nature, 474 (7352), 502-5 PMID: 21593762
Lukeš J, Archibald JM, Keeling PJ, Doolittle WF, & Gray MW (2011). How a neutral evolutionary ratchet can build cellular complexity. IUBMB life, 63 (7), 528-37 PMID: 21698757
What mutation rate do I want for my experiment?
18 hours ago in RRResearch