title: 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 CTXphi, a temperate filamentous phage that infects Vibrio cholerae and encodes cholera toxin. In CTXphi lysogens, the activity of P(rstA), the only CTXphi promoter required for CTX prophage development, is repressed by RstR, the CTXvphi repressor. We found that the V. cholerae SOS response regulates CTXvphi production. The molecular mechanism by which this cellular response to DNA damage controls CTXphi production differs from that by which the E. coli SOS response controls induction of many prophages. UV-stimulated CTXphi 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, CTXphi production is controlled by a cellular repressor whose activity is regulated by the cell's response to DNA damage.
authors.affiliation: Department of Molecular Microbiology, Tufts University School of Medicine and The Howard Hughes Medical Institute, Boston, MA 02111, USA.
authors.forename: Mariam
authors.initials: M
authors.lastname: Quinones
authors.forename: Harvey H
authors.initials: HH
authors.lastname: Kimsey
authors.forename: Matthew K
authors.initials: MK
authors.lastname: Waldor
mesh_terms: D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001435:Bacteriophages / Q000378:metabolism*; D001483:Base Sequence; D001665:Binding Sites; D002772:Cholera Toxin / Q000235:genetics / Q000378:metabolism*; D004249:DNA Damage; D004260:DNA Repair; D015964:Gene Expression Regulation, Bacterial; D016685:Mitomycin / Q000494:pharmacology; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D039002:Prophages / Q000378:metabolism*; D011485:Protein Binding; D011938:Rec A Recombinases / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D013014:SOS Response, Genetics; D012697:Serine Endopeptidases / Q000235:genetics / Q000378:metabolism*; D014466:Ultraviolet Rays; D014734:Vibrio cholerae / Q000187:drug effects / Q000235:genetics / Q000378:metabolism* / Q000528:radiation effects; D014775:Virus Activation; D000099160:LexA Repressor Protein
chemical_list: D000903:Antibiotics, Antineoplastic; D001426:Bacterial Proteins; D002772:Cholera Toxin; D016685:Mitomycin; D011938:Rec A Recombinases; D012097:Repressor Proteins; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein; C107871:RstR protein, Vibrio cholerae