INDUCTION OF THE SOS RESPONSE INCREASES THE EFFICIENCY OF GLOBAL NUCLEOTIDE EXCISION-REPAIR OF CYCLOBUTANE PYRIMIDINE DIMERS, BUT NOT 6-4-PHOTOPRODUCTS, IN UV-IRRADIATED ESCHERICHIA-COLI

Nucleotide excision repair (NER) is responsible for the removal of a v ariety of lesions from damaged DNA and proceeds through two subpathway s, global repair and transcription-coupled repair. In Escherichia coli , both subpathways require UvrA and UvrB, which are induced following DNA damage as part of the SOS response. We found that elimination of t he SOS response either genetically or by treatment with the transcript ion inhibitor rifampin reduced the efficiency of global repair of the major W-induced lesion, the cyclobutane pyrimidine dimer (CPD), but Ra d no effect on the global repair of 6-4 photoproducts. Mutants in whic h the SOS response was constitutively derepressed repaired CPDs more r apidly than did wild type cells, and this rate was not affected by rif ampin, Transcription-coupled repair of CPDs occurred in the absence of SOS induction but was undetectable when the response was expressed co nstitutively. These results suggest that damage-inducible synthesis of UvrA and UvrB is necessary for efficient repair of CPDs and that the levels of these proteins determine the rate of NER of UV photoproducts . We compare our findings with recent data from eukaryotic systems and suggest that damage-inducible stress responses are generally critical for efficient global repair of certain types of genomic damage.