Programmed cell death (PCD) occurs in both unicellular and multicellular organisms. While PCD plays a key role in the development and maintenance of multicellular organisms, explaining why single-celled organisms would evolve to actively commit suicide has been far more challenging. Here, we explore the potential for PCD to act as an accessory to microbial bet-hedging strategies that utilize stochastic phenotype switching. We consider organisms that face unpredictable and recurring disasters, in which fitness depends on effective phenotypic diversification. We show that when reproductive opportunities are limited by carrying capacity, PCD drives population turnover, providing increased opportunities for phenotypic diversification through stochastic phenotype switching. The main cost of PCD, providing resources for growth to a PCD(-) competitor, is ameliorated by genetic assortment in spatially structured populations. Using agent-based simulations, we explore how basic demographic factors, namely bottlenecks and local dispersal, can generate sufficient spatial structure to favor the evolution of high PCD rates.
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The authors thank the Chris Adami and two anonymous referees for their insightful comments-it greatly improved the paper. E.L. was supported by a SFI Omidyar fellowship. W.C.R. was supported by a Packard Foundation Fellowship for Science and Engineering and NSF grant #DEB-1456652.