“…Specifically, mutants of ~· coli wh~ch are defect~ve ~n recA· or lexA gene products are unable to induce this error-prone repair system (3,41,42). In addition to error-prone inducible post-replication repair, recA and/or lexA (exrA) mutations prevent error-prone excision ~epair (18), induction of ~ai~ophages (43,44), the induction of the recA gene product [formerly called protein X; (3,45,46,47)] the inhibition of exonuclease V (48), W-or UV reactivation, and W-mutagenesis (3,41,49,50), as well as other physiological changes following the inhibition of DNA replication and/or damage of the DNA (51). The pleiotropic effects of these mutations led Radman (52) to propose the 'SOS' hypothesis.…”