The sbcDC locus mediates repression of type 5 capsule production as part of the SOS response in Staphylococcus aureus.
Most strains of Staphylococcus aureus produce one type of capsular polysaccharide that belongs to either type 5 or type 8. The production of these capsules has been shown to be regulated by various regulators. Here we report that the sbcD and sbcC genes are involved in the repression of type 5 capsule production. Chromosomal deletions in the sbcDC genes resulted in increased capsule promoter activity, capsule gene transcripts, and capsule production. The survival rates of the sbcDC deletion mutant were reduced upon UV irradiation compared to those for the wild-type strain Newman, suggesting that the genes are involved in DNA repair in S. aureus. The two genes were organized as an operon and were expressed very early in the exponential growth phase. A subinhibitory concentration of ciprofloxacin or mitomycin C induced sbcDC transcription but repressed the capsule promoter activity, suggesting that the sbcDC genes and the capsule genes are part of the SOS regulon. By reporter gene fusion and Northern blotting, we found that sbcDC regulated capsule by downregulating arl and mgr. Further genetic studies indicate that sbcDC functions upstream of arl and mgr in capsule regulation. Collectively, our results indicate that sbcDC, upon the SOS response, represses type 5 capsule production through an arl-mgr pathway. To our knowledge, this is the first demonstration that an SbcDC homolog was involved in transcriptional regulation.
Chen
Zhongyi
Z
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Luong
Thanh T
TT
Lee
Chia Y
CY
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D019677:Artificial Gene Fusion; D016667:Bacterial Capsules / Q000096:biosynthesis*; D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D015152:Blotting, Northern; D015153:Blotting, Western; D002939:Ciprofloxacin / Q000494:pharmacology; D003851:Deoxyribonucleases / Q000235:genetics / Q000502:physiology*; D005092:Exonucleases / Q000235:genetics / Q000502:physiology*; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D017930:Genes, Reporter; D050296:Microbial Viability; D016685:Mitomycin / Q000494:pharmacology; D011401:Promoter Regions, Genetic; D012329:RNA, Bacterial / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D012097:Repressor Proteins / Q000235:genetics / Q000502:physiology*; D013014:SOS Response, Genetics; D013211:Staphylococcus aureus / Q000235:genetics* / Q000502:physiology / Q000528:radiation effects; D014158:Transcription, Genetic / Q000187:drug effects; D014466:Ultraviolet Rays; D001616:beta-Galactosidase / Q000096:biosynthesis / Q000235:genetics
D000900:Anti-Bacterial Agents; C411334:ArlR protein, Staphylococcus aureus; D001426:Bacterial Proteins; D012329:RNA, Bacterial; D012333:RNA, Messenger; D012097:Repressor Proteins; C061563:SbcC protein, Bacteria; D016685:Mitomycin; D002939:Ciprofloxacin; D003851:Deoxyribonucleases; D005092:Exonucleases; D001616:beta-Galactosidase
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