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Biomedical subjects

Katherine A Schmidt

Publications and source records attributed to Katherine A Schmidt.

2 recordsLinked to original sources

Influences of sigmaB and agr on expression of staphylococcal enterotoxin B (seb) in Staphylococcus aureus.

In Staphylococcus aureus, enterotoxin B (SEB) is a superantigen that activates host interleukins and induces adverse responses, ranging from food poisoning to toxic shock. The alternate sigma factor, sigmaB (SigmaB), and agr are two known regulators of S. aureus. Northern blots of strain COL, a sigB-positive strain, showed an inverse correlation between sigmaB expression and seb message. seb expression was also measured as a function of a seb promoter linked to green fluorescent protein (GFP) expression in RN6390, COL, and Newman. In sigB mutants of RN6390, SH1000, COL, and Newman, seb promoter activities, as measured by GFP expression, increased relative to the respective parental types but at differing levels, suggesting alternate strain-specific regulation. In agr mutants of RN6390 and Newman, seb promoter activities were intermediate between the high level seen for the sigB mutant and the low level in the sigB active strains. A sigB agr double mutant of RN6390 displayed lower GFP expression than the agr mutant. These results suggest that while sigmaB and agr regulate seb expression in a divergent manner, other activator(s) of seb that depend on sigB expression may be present in S. aureus.

Bacterial Proteins↗

SarT influences sarS expression in Staphylococcus aureus.

Staphylococcus aureus is a gram-positive pathogen that is capable of expressing a variety of virulence proteins in response to environmental signals. Virulence protein expression in S. aureus is controlled by a network of regulatory loci including sarA and agr. The sarA/agr network is associated with the expression of cell wall-associated adhesins during exponential growth and the expression of secreted enzymes and toxins in the transition to post-exponential growth. A number of sarA homologs, including sarT and sarS, have been identified in the S. aureus genome. Previous studies have shown that sarA influences expression of both sarT and sarS in the global regulatory network. SarS has been shown to bind to the spa promoter to induce expression of protein A. SarT, one of the SarA homologs that represses hla expression and is repressible by SarA and agr, was found to induce sarS expression in this report. Northern blot analysis of sarS and spa expression in S. aureus RN6390, and the isogenic sarT, sarT sarA, and sarT agr mutants showed that while sarA regulated spa expression directly, the agr locus used sarT as an intermediary to regulate sarS, thus leading to spa repression in agr-activated cells. Gel shift and footprinting analysis showed that SarT binds to the sarS promoter, indicating that the interaction of the sarT gene product with the upstream region of sarS is likely direct. Induction of sarS and spa by SarT in agr(+) strains was confirmed by a tetracycline-inducible system to titrate sarT expression.

Antigens, Bacterial↗