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To evaluate the role of SigB in modulating the expression of virulence determinants inStaphylococcus aureus , we constructed asigB mutant of RN6390, a prototypicS. aureus strain. The mutation in thesigB gene was confirmed by the absence of the SigB protein in the mutant on an immunoblot as well as the failure of the mutant to activate ςB-dependent promoters (e.g., thesarC promoter) ofS. aureus . Phenotypic analysis indicated that both alpha-hemolysin level and fibrinogen-binding capacity were up-regulated in the mutant strain compared with the parental strain. The increase in fibrinogen-binding capacity correlated with enhanced expression of clumping factor and coagulase on immunoblots. The effect of thesigB mutation on the enhanced expression of the alpha-hemolysin gene (hla ) was primarily transcriptional. Upon complementation with a plasmid containing thesigB gene,hla expression returned to near parental levels in the mutant. Detailed immunoblot analysis as well as a competitive enzyme-linked immunosorbent assay of the cell extract of thesigB mutant with anti-SarA monoclonal antibody 1D1 revealed that the expression of SarA was higher in the mutant than in the parental control. Despite an elevated SarA level, the transcription of RNAII and RNAIII of theagr locus remained unaltered in thesigB mutant. Because of a lack of perturbation inagr , we hypothesize that inactivation ofsigB leads to increased expression of SarA which, in turn, modulates target genes via anagr -independent but SarA-dependent pathway.

Hyperproduction of Alpha-Hemolysin in a sigB Mutant Is Associated with Elevated SarA Expression in Staphylococcus aureus