GENETIC-EVIDENCE FOR AN ACTIVATOR REQUIRED FOR INDUCTION OF COLICIN-LIKE BACTERIOCIN 28B PRODUCTION IN SERRATIA-MARCESCENS BY DNA-DAMAGING AGENTS

Citation
S. Ferrer et al., GENETIC-EVIDENCE FOR AN ACTIVATOR REQUIRED FOR INDUCTION OF COLICIN-LIKE BACTERIOCIN 28B PRODUCTION IN SERRATIA-MARCESCENS BY DNA-DAMAGING AGENTS, Journal of bacteriology, 178(4), 1996, pp. 951-960
Citations number
58
Categorie Soggetti
Microbiology
Journal title
ISSN journal
00219193
Volume
178
Issue
4
Year of publication
1996
Pages
951 - 960
Database
ISI
SICI code
0021-9193(1996)178:4<951:GFAARF>2.0.ZU;2-C
Abstract
Bacteriocin 28b production is induced by mitomycin in wild-type Serrat ia marcescens 2170 but not in Escherichia coli harboring the bacterioc in 28b structural gene (bss). Studies with a bss-lacZ transcriptional fusion showed that mitomycin increased the level of bss gene transcrip tion in S. marcescens but not in the E. coli background, A S. marcesce ns Tn5 insertion mutant was obtained (S. marcescens 2170 reg::Tn5) who se bacteriocin 28b production and bss gene transcription were not incr eased by mitomycin treatment, Cloning and DNA sequencing of the mutate d region showed that the Tn5 insertion was flanked by an SOS box seque nce and three genes that are probably cotranscribed (regA, regB, and r egC), These three genes had homology to phage holins, phage lysozymes, and the Ogr transcriptional activator of P2 and related bacteriophage s, respectively, Recombinant plasmid containing this wild-type DNA reg ion complemented the reg::TnS regulatory mutant, A transcriptional fus ion between a 157-bp DNA fragment, containing the apparent SOS box ups tream of the regA gene, and the caf gene showed increased chlorampheni col acetyltransferase activity upon mitomycin treatment, Upstream of t he bss gene, a sequence similar to the consensus sequence proposed to bind Ogr protein was found, but no sequence similar to an SOS box was detected. Our results suggest that transcriptional induction of bacter iocin 28b upon mitomycin treatment is mediated by the regC gene whose own transcription would be LexA dependent.