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Jolivet, E.*; Lecointe, F.*; Coste, G.*; Sato, Katsuya*; Narumi, Issei; Bailone, A.*; Sommer, S.*
Molecular Microbiology, 59(1), p.338 - 349, 2006/01
Times Cited Count:40 Percentile:57.25(Biochemistry & Molecular Biology)To evaluate the importance of RecA in DNA double strand break (DSB) repair, we examined the effect of low and high RecA concentration such as 2,500 and 100,000 molecules per cell from the inducible P promoter in in absence or in presence of IPTG, respectively. We showed that at low concentration, RecA has a negligible effect on cell survival after -irradiation when bacteria were immediately plated on TGY agar whereas it significantly decreased the survival to -irradiation of cells while overexpression of RecA can partially compensate the loss of DdrA protein. In contrast, when cells expressing limited concentration of RecA were allowed to recover in TGY liquid medium, they showed a delay in mending DSB, failed to reinitiate DNA replication and were committed to die during incubation in liquid medium. A deletion of resulted in sensitivity to -irradiation and mitomycin C treatment. Interestingly, constitutive high expression of RecA compensates partially the sensitization to mitomycin C. The cells with low RecA content also failed to cleave LexA after DNA damage. However, neither a deletion of the gene nor the expression of a non cleavable LexA(Ind) mutant protein, had an effect on survival or kinetics of DNA DSB repair compared to their counterparts in as well as in bacteria expressing limiting concentration of RecA, suggesting an absence of relationship between the loss of viability, the delay in the kinetic of DSB repair, and the absence of LexA cleavage. Thus, LexA protein seems to play no major role in the recovery processes after -irradiation in .
Narumi, Issei; Sato, Katsuya; Cui, S.*; Funayama, Tomoo; Kitayama, Shigeru; Watanabe, Hiroshi*
Molecular Microbiology, 54(1), p.278 - 285, 2004/10
Times Cited Count:133 Percentile:91.37(Biochemistry & Molecular Biology)The extraordinary radiation resistance of results from the efficient capacity of the bacterium to repair DNA double-strand breaks. By analyzing the DNA damage repair-deficient mutant, KH311, a unique radiation-inducible gene (designated ) responsible for loss of radiation resistance was identified. Investigations in vitro showed that the gene product of (PprA) preferentially bound to double-stranded DNA carrying strand breaks, inhibited exonuclease III activity, and stimulated the DNA end-joining reaction catalyzed by ATP-dependent and NAD-dependent DNA ligases. These results suggest that has a radiation-induced nonhomologous end-joining repair mechanism in which PprA plays a critical role.