ONE INCOMPLETELY understood puzzle in evolutionary theory is what is the driving force for greater complexity in a living system. Intelligent design proponents are heavily invested in the idea of complexity but disagree on how to measure it, with most measurements coming down to basic biomass. This is a poor means of measuring complexity, but the reasons for this are outside the scope of this article (for a short summary of some concepts in biological complexity see this article, sadly only available to subscribers). However, when considering a biological pathway we can probably agree that a pathway with only a few proteins is less complex than a pathway that fulfills the same role but uses many more proteins. Consider the clotting cascade. In simple chordates such as Amphioxus possibly only two or three proteins are involved (we don’t know the full details), while in mammals there are more than a dozen components. Research has demonstrated that the clotting system is not irreducibly complex, but the reason for this increase in complexity has not been previously determined.

A new open-access article in PNAS helps answer this question. The authors modeled a signaling pathway of three proteins under selection in a variety of conditions (selection is required, when modeled without selection the pathway soon became extinct, as would be predicted). Their results suggest that such pathways should evolve to be larger than actually required for their role due to a ratchet effect in mutation of the pathway. Generally, additions to the pathway were less likely to be detrimental than deletions, and as the pathways grew larger deletions were less likely to destroy the pathway. This mimics what is seen in nature in which complex systems often still are functional if one of the components is knocked out. Thus the growth in complexity in an enzymatic pathway is not due to any force driving the development of the pathway, but by mutation’s passive addition of components (even those without an immediate benefit) building greater complexity and the stabilizing effect of redundancy once a certain size is reached.

Soyer, O.; Bonhoeffer, S. “Evolution of complexity in signaling pathways.” Proceedings of the National Academy of Sciences, USA. 2006, 103, 16337-16342.
Szathmáry, E.; Jordán, F.; Pál, C. “Can genes explain biological complexity?” Science. 2001, 292, 1315-1316.