Fig. 8: Induction of the staphylococcal SOS response and prophages.

DNA damage activates the RecA (RecA*) protein which binds to both the LexA and the CI repressor catalysing their autocleavage. The repressor N-terminal domains retain some DNA-binding capacity. ClpX specifically binds to the N-terminal repressor domains after RecA* catalysed cleavage. For SOS induction, ClpX needs to interact with ClpP to facilitate the proteolytic degradation of the LexA N-terminus. This then also results in the increased expression of RecA further increasing SOS induction for as long as DNA damage is present. By contrast, prophage induction does not require the interaction of ClpX and ClpP and binding of ClpX to the N-terminal fragment of CI is sufficient for inducting the lytic phage cycle.