The gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The 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 gene is observed in both the Δ Δ cells and cells, and a fivefold increase in the Δ Δ cells relative to the wild-type cells. The full activity of the promoter region requires both the p1-2 and p3 promoters and is repressed by both the DnaA and LexA proteins. LexA binds tightly to LexA-box1 at the p1-2 promoter irrespective of the presence of DnaA and this binding is important for the control of the p1-2 promoter. DnaA and LexA, however, compete for binding to and regulation of the p3 promoter in which the DnaA-box6 overlaps with LexA-box4. The transcription control of p3 largely depends on DnaA-box6. Transcription of other SOS regulon genes, such as and , is also repressed by both DnaA and LexA. Interestingly, the absence of LexA in the presence of the DnaA 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.