**Abstract**

The *Escherichia coli* SOS response is an inducible DNA damage repair pathway controlled by two key regulators, LexA, a repressor and RecA, an inducer. Upon DNA damage RecA is activated and stimulates self cleavage of LexA, leading to, in *E. coli,* derepresion of approximately 50 SOS genes. The response is triggered by exogenous and endogenous signals that bacteria encounter at a number of sites within the host. Nevertheless, besides regulating DNA damage repair the SOS response plays a much broader role. Thus, SOS error prone polymerases promote elevated mutation rates significant for genetic adaptation and diversity, including antibiotic resistance. Here we review the *E. coli* SOS response in relation to recalcitrance to antimicrobials, including persister and biofilm formation, horizontal gene tranfer, gene mobility, bacterial pathogenicity, as well SOS induced bacteriocins that drive diversification. Phenotypic heterogeneity in expression of the SOS regulator genes, *recA* and *lexA* as well as colicin activity genes is also discussed.

**Keywords:** SOS response, *Escherichia coli*, DNA damage, antibiotic resistance, persisters, horizontal gene transfer, virulence, biofilms, bacteriocins, phentypic heterogeneity
