Many of the DNA damage-inducible genes encoding DNA repair and recombination proteins are expressed as part of the SOS response (39, 40). LexA protein represses the genes of the SOS regulon (Table 1); when DNA damage occurs, RecA protein inactivates the LexA repressor, leading to induction of the SOS response. The SOS response controls the expression of genes involved in recombination repair (daughter-strand gap repair, double-strand break repair), excision repair (both short and long patch), mutagenesis (error-prone repair), and mismatch repair of DNA. This review will focus on recent data pertaining to DNA repair and mutagenesis associated with expression of the SOS response. The presence of DNA damage may be lethal unless the repair and recombination potential of the cell is increased. Many lesions resulting from DNA-damaging treatments or stalled DNA replication require derepression of the SOS response for their repair or bypass. The damage sites themselves and/or the products of preinduction processing may serve as signals to activate RecA so that SOS functions may be derepressed (34). The various repair systems under control of the SOS regulon then act directly to repair the original lesions or allow the cell to tolerate the lesions until repair can be effected by other mechanisms.