Considering Cellular Complexity

It is challenging to account for the origins or fully fathom the workings of the generally imposing and sometimes inspiring complexity of both intracellular and extracellular biochemical systems.  One theme among many illustrative of this complexity is the mediation of key functions such as signal transduction from the cell surface, gene transcription, mRNA processing, and translation of mRNA into protein by large assemblies of as many as hundreds of gene products (i.e., proteins or proteins and RNA molecules). A recent commentary in Science (Gray et al., 2010) offers an interesting hypothesis to account for some of what the authors refer to as the irremediable complexity of molecular biological systems. This evolutionary mechanism turns on the presumed asymmetry inherent in the probabilities of mutations either reversing or stabilizing a new intermolecular interaction created by a preceding genetic alteration. 

The essence of the mechanism proposed by Gray and colleagues can be summarized as follows by considering two gene products, A and B. Initially, A and B do not physically interact. Imagine that a spontaneous mutation then happens to the gene encoding A and that this amino acid substitution newly permits A to physically associate with B without undermining the separate functions of A or B. (If such a mutation did subvert the function of either A or B it would presumably be selected against.)  Gray et al. argue that the association of A with B may permit some otherwise A-inactivating mutations to occur without loss of function by A, thereby selecting against a reversion to independence of A from B.  Thus, mutations affecting A that are only tolerated if A interacts with B, could accumulate.  The authors liken this sort of process to a mechanical ratchet for which motion in one direction is much more likely than motion in the reverse direction.    
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In the view of Gray et al., the sorts of mutations just described can be, at least frequently enough, selectively neutral.  If so, then it is possible that much of the complexity that prompts others to construct evolutionary scenarios that presuppose a fundamentally adaptive process might have arisen through a largely non-selective pathway.  As initiatives in both systems and synthetic biology move forward, opportunities to assess the significance of the mechanism for the generation of complexity proposed by Gray et al. should be forthcoming.
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Many readers of EMR will have heard the claim, by proponents of the notion that organisms are the products of a presumably supernatural designer of unknown identity, location, or methodology, that cellular systems are too complex to have evolved.  In this context, one ironic implication of the neutral ratchet mechanism of complexification is that, contrary to the claims of these anti-evolutionists, cellular complexity instead of being too complex to have  evolved may be too gratuitously complex to have been designed, at least by any agent that has any purpose other than mere amusement in mind.
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On the other hand, this line of thinking, that biology pointlessly overcomplicates all systems can be taken too far.  In an original and absorbing account of how structures extraneous to the normally-conceived boundaries of organisms (e.g., captive air bubbles used by water-dwelling spiders and beetles for breathing) can nevertheless crucially contribute to routine physiology, Turner (2000) offers a thesis he refers to as “Goldberg’s lever:”

“Indeed, biology is so full of seemingly claptrap solutions to rather simple problems that I would not simply reject Occam’s razor as a usefil tool in biology. I would go further and pose a new philosophical rule, that the more complicated the explanation, the more likely it is to be true. We can call it, for lack of a better name, Goldberg’s lever, after the cartoonist Rube Goldberg and his ingeniously complicated solutions to simple problems.” 

Clearly, any explanation of a biological process or phenomenon, however complex, could be made both more complex and less accurate if care is not taken to adhere closely to the constraints imposed by reality.  The ratchet of Gray et al. notwithstanding, at some point, I expect that the burdens inevitably imposed by additional mechanistic complexity that fails to advance fitness will elicit the ruthless simplification associated with negative selection.   

References

Gray MW, Lukes J, Archibald JM, Keeling PJ, Doolittle WF. Cell biology. Irremediable complexity? Science. 2010 Nov 12;330(6006):920-1. PubMed PMID:21071654.

Turner, J. Scott. The Extended Organism: The Physiology of Animal-Built Structures. Harvard University Press, 2000.