The genetic basis for the evolution of altruism during the transition to multicellularity

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Altruism - the capacity to perform acts costly to self but beneficial to others, is central to the evolution of various biological phenomena from social behavior to evolutionary transitions in individuality. Although the selective conditions favoring altruism are being increasingly understood, the evolutionary origins of the genetic basis for this behavior remain elusive. The most extreme forms of altruism are reproductive altruism and suicide. In multicellular organisms, they are typified by the differentiation of sterile somatic cells during development and the launch of the cell suicide program in damaged or mutated cells. The goal of this research program is to investigate the genetic basis for the evolution of reproductive altruism (i.e., soma) and cell suicide (programmed cell death, PCD) during the transition to multicellularity. Our general hypothesis is that the evolution of altruism involved the co-option of genes and modification of regulatory circuits implicated in the response to changing/stressful environments. The finding that the evolution of altruism during the evolution of multicellularity involved the co-option of a regulatory pathway conditioned on environmental cues will (i) complement and provide support to recent proposals that cast differentiation and social evolution involved the remodeling of regulatory circuits associated with the perception/processing of environmental stimuli by solitary organisms, and (ii) argue that general principles underlying the evolution of altruism at the molecular level can be identified. In addition, information on the evolution of PCD will facilitate our understanding of signaling pathways regulating PCD and cell proliferation and can improve our ability to predict the consequences of perturbations in these pathways in complex multicellular organisms, including humans.