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The LexA regulated SOS network is a bacterial response to DNA damage of metabolic or environmental origin. In  Clostridium difficile , a nosocomial pathogen causing a range of intestinal diseases, the  in-silico  deduced LexA network included the core SOS genes involved in the DNA repair and genes involved in various other biological functions that vary among different ribotypes. Here we describe the construction and characterization of a  lexA  ClosTron mutant in  C .  difficile  R20291 strain. The mutation of  lexA  caused inhibition of cell division resulting in a filamentous phenotype. The  lexA  mutant also showed decreased sporulation, a reduction in swimming motility, greater sensitivity to metronidazole, and increased biofilm formation. Changes in the regulation of toxin A, but not toxin B, were observed in the  lexA  mutant in the presence of sub-inhibitory concentrations of levofloxacin.  C .  difficile  LexA is, therefore, not only a regulator of DNA damage but also controls many biological functions associated with virulence.

The SOS Response Master Regulator LexA Is Associated with Sporulation, Motility and Biofilm Formation in Clostridium difficile