LexA Cleavage Is Required for CTX Prophage Induction

Abstract

The physiologic conditions and molecular interactions that control phage production have been studied in few temperate phages. We investigated the mechanisms that regulate production of CTXφ, a temperate filamentous phage that infects Vibrio cholerae and encodes cholera toxin. In CTXφ lysogens, the activity of P rstA , the only CTXφ promoter required for CTX prophage development, is repressed by RstR, the CTXφ repressor. We found that the V. cholerae SOS response regulates CTXφ production. The molecular mechanism by which this cellular response to DNA damage controls CTXφ production differs from that by which the E. coli SOS response controls induction of many prophages. UV-stimulated CTXφ production required RecA-dependent autocleavage of LexA, a repressor that controls expression of numerous host DNA repair genes. LexA and RstR both bind to and repress P rstA . Thus, CTXφ production is controlled by a cellular repressor whose activity is regulated by the cell's response to DNA damage.