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Evolution of individuality

The origin of multicellular life is probably the premiere example of the integration of lower levels in the biological hierarchy into a new higher level evolutionary unit. According to Jablonka and Lamb, “the EISs that evolved in early unicellular organisms probably played an important role in the transition of multicellularity”. In my commentary, I focus on the transition from single cell to multicellular organisms. The emergence of organisms as a new evolutionary unit depends in part upon the power of group selection promoting greater levels of cooperativity and synergism among cells. For this to happen, selection at the lower level, selection among cells, must be controlled; if not, selfish mutants may arise which threaten the existence of the emerging higher level entity, the organism. The main basis for the author’s claim that EISs promote the transition to multicellular life is that EISs make it easier for group selection to over power selection at the cell level. Specifically, they argue that selfish mutants are less likely in the presence of established EISs. “For a mutant cell to destroy the coherence of a group, it must forget its epigenetic heritage and defy the inductive influences of other members of the group, as well as proliferate more rapidly than its neighbours. The validity of these ideas about the importance of EISs in the evolution of multicellularity can be tested by modelling conipetition between groups of mutation cells with and without epigenetic inheritance” (p. 20). I have studied mutational models of the transition between unicellular and multicellular life (Michod, 1997a; Michod, 1997b; Michod and Roze, 1997; Michod, 1996), but not ones with epigenetic inheritance. Jablonka and Lamb’s article has stimulated me to extend my models to include an EIS which I am in the process of doing. I feel Jablonka and Lamb’s conjecture may be correct EISs may help retard selfish mutants. However, I wonder about the risks of mutations in marker genes that are responsible for turning structural genes on and off (for example, mutations in genes responsible for states of methylation). If I understand Jablonka