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Abstract  Phenotypic diversity provides populations of prokaryotic and eukaryotic organisms with the flexibility required to adapt to and/or survive environmental perturbations. Consequently, there is much interest in unraveling the molecular mechanisms of heterogeneity. A classical example of heterogeneity inEscherichia coliis the subset (3%) of the population that expresses the colicin K activity gene (cka) upon nutrient starvation. Here, we report on the mechanism underlying this variable response. As colicin synthesis is regulated by the LexA protein, the central regulator of the SOS response, we focused on the role of LexA and the SOS system in the variableckaexpression. Real-time RT-PCR showed that the SOS system, without exogenous DNA damage, induces moderate levels ofckaexpression. The use ofcka–gfpfusions demonstrated that modification of the conserved LexA boxes in theckapromoter region affected LexA binding affinity and the percentage ofcka–gfpexpressing cells in the population. AlexA–gfpfusion showed that thelexAgene is highly expressed in a subset of bacteria. Furthermore, cka–gfpfusions cloned into higher copy plasmid vectors increased the percentage ofcka–gfppositive bacteria. Together, these results indicate that the bistability inckaexpression in the bacterial population is determined by (1) basal SOS activity, (2) stochastic factors and possibly (3) the interplay of LexA dimers atckaoperator. Other LexA regulated processes could exhibit similar regulation. [ABSTRACT FROM AUTHOR]