Evolution of Cellular Complexity
Michael R. Lynch · 2024
Abstract Natural selection is expected to favor simplicity over more complex features, provided their functionality is similar, owing to the increased energetic costs and mutational vulnerability of the latter. However, many aspects of eukaryotic cell biology are overdesigned, particularly in multicellular species. Such evolution can be explained by the operation of constructive neutral evolution in populations of sufficiently small size. Under this hypothesis, the fortuitous development of weakly deleterious gene–product interactions can secondarily mask the more deleterious effects of previously forbidden mutations, thereby leading to a ratchet-like increase in complexity. The substantial expansions of the number of subunits in ribosomes and ETC complexes in eukaryotes, with no obvious increase in performance relative to prokaryotes, are potential examples of this process. Gene duplication also provides a route to the origin of evolutionary novelties, with one copy being free to evolve a new function. However, the commoner outcome of gene duplication is the partitioning of ancestral-gene subfunctions among the offspring genes by complementary degenerative mutations. Along with the development of the modular gene structure upon which it depends, this process of subfunctionalization has an elevated probability of operation in populations with reduced effective sizes. Gene duplication also provides a powerful mechanism for speciation, as it results in reassignments of gene functions to different chromosomal locations. Thus, although superficially appearing adaptive in nature, the emergence of organismal complexity, as well as the creation of reproductively isolated lineages, is often a passive outcome of non-adaptive processes that prevail in populations of sufficiently small size.