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Updated: Jun 4, 2026

Following Cell-fate in E. coli After Infection by Phage Lambda
Published on: October 14, 2011
The adaptive plasticity of temperate phage λ
Sylvain Gandon1, Tapan Goel2, Joshua S Weitz2,3
1CEFE, CNRS, Univ Montpellier, EPHE, IRD, Montpellier, France.
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When the temperate phage [Formula: see text] infects its host, the bacterium Escherichia coli, it can either replicate to form new progeny (lytic growth) or integrate its genome into the host chromosome (lysogenization). Crucially, the probability of lysis or lysogeny is tightly regulated and varies with phage and host genotypes and the environment. In particular, the number of viruses coinfecting the same host cell is known to have a strong effect on the outcome of the infection, leading to phenotypic plasticity: the probability of lysogenization is higher when the cellular multiplicity of infection (MOI) increases. However, the selective forces driving the evolution of plasticity in phage [Formula: see text] remain unclear. Here, we analyze the evolution of the plasticity of lysogenization and show that a MOI-varying strategy is adaptive when the abundance of susceptible cells fluctuates periodically. We study how the speed of these fluctuations and various within-host decision rules affect the evolution of viral plasticity. Our results suggest that the complex genetic regulation of lysogeny in temperate phages can be shaped by natural selection allowing viruses to use the MOI as indirect information to persist in environments with fluctuating host densities.
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