The SOS-dependent upregulation of uvrD is not required for efficient nucleotide excision repair of ultraviolet light induced DNA photoproducts in Escherichia coli

We have shown previously that induction of the SOS response is required for efficient nucleotide excision repair (NER) of the major ultraviolet light (UV) induced DNA lesion, the cyclobutane pyrimidine dimer (CPD), but not fo r repair of 6-4 photoproducts (6-4PP) or for transcription-coupled repair o f CPDs [1]. We have proposed that the upregulation of cellular NER capacity occurs in the early stages of the SOS response and enhances the rate of re pair of the abundant yet poorly recognized genomic CPDs. The expression of three NER genes, uvrA, uvrB, and uvrD, is upregulated as part of the SOS re sponse. UvrD differs from the others in that it is not involved in lesion r ecognition but rather in promoting the post-incision steps of NER, includin g turnover of the UvrBC incision complex. Since uvrC is not induced during the SOS response, its turnover would seem to be of great importance in prom oting efficient NER. Here we show that the constitutive level of UvrD is ad equate for carrying out efficient NER of both CPDs and 6-4PPs. Thus, the up regulation of uvrA and uvrB genes during the SOS response is sufficient for inducible NER of CPDs. We also show that cells with a limited NER capacity , in this case due to deletion of the uvrD gene, repair 6-4PPs but cannot p erform transcription-coupled repair of CPDs, indicating that the 6-4PP is a better substrate for NER than is a CPD targeted for transcription-coupled repair. (C) 2001 Elsevier Science B.V. All rights reserved.