Inhibition of cell division in Escherichia coli by ultraviolet radiation
The inhibition of cell division after UV in wild-type bacteria is considered to be an "SOS" function under the control of recA; this control was the subject of the investigation. A kinetic study of division inhibition and recA synthesis after a low dose of UV indicated that recA did hot act directly to inhibit division. Further, recA synthesis was uncoupled from the division block in the presence of low levels of rifampicin. Nevertheless, recA is essential for division inhibition after UV. A Ion mutant, which unlike Ion strains did not recover from the division block, showed no alteration in the kinetics of recA induction. A mutation in a second gene, sulB, suppressed the lethal effect of UV on Ion mutants by promoting recovery after a period of division inhibition; possible mechanisms of suppression are considered. To investigate .the interaction between sulB, recA and Ion at the molecular level, a transducing phage was obtained carrying the proposed sulB region of the chromosome. The transducing DNA was recloned into a plasmid vector and a strain containing the recombinant plasmid showed an altered division response after UV, suggesting that a division control gene was present in the cloned DNA. Gene products coded by the transducing phage and the recombinant plasmids were demonstrated by in vitro and semi-in vivo techniques and the m vitro systems was developed further with the object of detecting possible transcriptional control of cloned genes by recA. The results are considered in the light of some recent developments having important implication's for the project.