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

Abstract

The <i>uvrB</i> gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The <i>uvrB</i> 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 <i>uvrB</i> gene is observed in both the Δ<i>lexA</i> Δ<i>sulA</i> cells and <i>dnaA</i>_A345S cells, and a fivefold increase in the Δ<i>lexA</i> Δ<i>sulA dnaA</i>_A345S cells relative to the wild-type cells. The full activity of the <i>uvrB</i> promoter region requires both the <i>uvrB</i>p1-2 and <i>uvrB</i>p3 promoters and is repressed by both the DnaA and LexA proteins. LexA binds tightly to LexA-box1 at the <i>uvrB</i>p1-2 promoter irrespective of the presence of DnaA and this binding is important for the control of the <i>uvrB</i>p1-2 promoter. DnaA and LexA, however, compete for binding to and regulation of the <i>uvrB</i>p3 promoter in which the DnaA-box6 overlaps with LexA-box4. The transcription control of <i>uvrB</i>p3 largely depends on DnaA-box6. Transcription of other SOS regulon genes, such as <i>recN</i> and <i>dinJ</i>, 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.