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The  uvrB  gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The  uvrB  promoter region contains three identified promoters with four LexA binding sites, one consensus and six potential DnaA binding sites. A more than threefold increase in transcription of the chromosomal  uvrB  gene is observed in both the Δ lexA  Δ sulA  cells and  dnaA  A345S  cells, and a fivefold increase in the Δ lexA  Δ sulA dnaA  A345S  cells relative to the wild-type cells. The full activity of the  uvrB  promoter region requires both the  uvrB p1-2 and  uvrB p3 promoters and is repressed by both the DnaA and LexA proteins. LexA binds tightly to LexA-box1 at the  uvrB p1-2 promoter irrespective of the presence of DnaA and this binding is important for the control of the  uvrB p1-2 promoter. DnaA and LexA, however, compete for binding to and regulation of the  uvrB p3 promoter in which the DnaA-box6 overlaps with LexA-box4. The transcription control of  uvrB p3 largely depends on DnaA-box6. Transcription of other SOS regulon genes, such as  recN  and  dinJ , is also repressed by both DnaA and LexA. Interestingly, the absence of LexA in the presence of the DnaA A345S  mutant leads to production of elongated cells with incomplete replication, aberrant nucleoids and slow growth. We propose that DnaA is a modulator for maintenance of genome integrity during the SOS response by limiting the expression of the SOS regulon.

DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon