The SOS response is a state of high-activity DNA repair, and is activated by bacteria that have been exposed to heavy doses of DNA-damaging agents. Their DNA is basically chopped to shreds, and the bacteria attempts to repair its genome at any cost (including inclusion of mutations due to error-prone nature of repair mechanisms). The SOS system is a regulon; that is, it controls expression of several genes distributed throughout the genome simultaneously.
The primary control for the SOS regulon is the gene product of lexA, which serves as a repressor for recA, lexA(which means it regulates its own expression), and about 16 other proteins that make up the SOS response. During a normal cellís life, the SOS system is turned off, because lexA represses expression of all the critical proteins. However, when DNA damage occurs, RecA binds to single-stranded DNA (single-stranded when a lesion creates a gap in daughter DNA). As DNA damage accumulates, more RecA will be bound to the DNA to repair the damage.
What is interesting is that RecA, in addition to its abilities in recombination repair, stimulates the autoproteolysis of lexAís gene product (*NOTE* I still need to do a bit more research on this, as to the mechanism). That is, LexA will cleave itself in the presence of bound RecA, which causes cellular levels of LexA to drop, which, in turn, causes coordinate derepression (induction) of the SOS regulon genes.
As damage is repaired, RecA releases DNA; in this unbound form, it no longer causes the autoproteolysis of LexA, and so the cellular levels of LexA rise to normal again, shutting down expression of the SOS regulon genes.