Effects of fluoro-phenyl-styrene-sulfonamide (FPSS) on transcription factor sigma B regulons in Staphylococcus aureus

Staphylococcus aureus has been shown to cause various types of tissue and systemic infections in humans and livestock with the mortality rate of 20-30%. Some isolates can be highly resistant to antibiotics hence the need to identify better drugs and drug targets. Previous studies have shown that (E)-N-(4-Fluorophenyl)-2-phenylethene sulfonamide (FPSS) could inhibit activities of a bacteria-specific transcription factor sigma B. Sigma B regulons in Bacillus subtilis and in Listeria monocytogenes, including virulence factor genes in L. monocytogenes, were decreased. Since sigma B is also presented in S. aureus, we initially postulated the use of FPSS to target S. aureus sigma B activity and to attenuate its virulence gene expression. Surprisingly, qRT-PCR results revealed that FPSS induced expression of sigma B-dependent gene asp23. RNAseq results showed 39 S. aureus genes were affected by FPSS (37 genes were downregulated and two genes were upregulated). FPSS had no effect on expression of sigB operon in S. aureus. To investigate the affect of FPSS on transcription factor sigma B regulons in Staphylococcus aureus by RNAseq