Dps Augments LexA Autocleavage after UV-C-Induced DNA Damage in Stationary Phase Escherichia coli

Ultraviolet radiation is known to induce bacterial DNA damage, resulting in the dimerization of thymine base pairs and the production of single stranded DNA. Several DNA repair mechanisms are currently known to exist in Escherichia coli. The genes encoding these repair systems belong to the SOS regulon. Normally the SOS-mediated DNA repair system is repressed by LexA. Upon detection of DNA damage, the active form of RecA facilitates the autocleavage of LexA, thereby inducing the global DNA repair response. The DNA-binding protein from starved cells (Dps) is known to protect DNA during starvation and environmental stress. Apart from structural protection, it has been speculated that Dps may play a regulatory role in DNA repair. To investigate the influence of Dps on the activation of the SOS repair system after UV-induced DNA damage, E. coli ZK126 (wild type) and ZK1146 ( dps mutant) were assayed immunologically for LexA cleavage. In the dps mutant, the repressor form of LexA monomers was not cleaved throughout the 3 minute time frame, compared to the observed decline in the wild-type sample, indicating a lack of RecA activation in the absence of Dps. The results of this study support the hypothesis that Dps plays a role in the induction of the SOS response.