Previous studies have shown that expression of aur (metalloprotease; aureolysin) and sspA (V8 protease; serine protease) in Staphylococcus aureus strain 8325-4 is maximal in the postexponential phase of growth, when the agr (RNAIII) system is activated. Transcription of aur and sspA is mainly regulated through repression by sarA and rot, and RNAIII stimulates protease production by inhibiting translation of rot mRNA. As SarR is a repressor of sarA, inactivation of sarR would result in downregulation of aur and sspA transcription. This was confirmed by mRNA analysis using quantitative real-time PCR. However, we found that sarR acted as a direct stimulator, i.e. its positive effect on aur and sspA transcription did not require sarA (or rot) per se. In addition, aur and sspA were dependent on sarR for maximal transcription. This stimulating role of sarR was not restricted to the rsbU-deficient laboratory strain 8325-4 but was also demonstrated in S. aureus strain SH1000 (rsbU-complemented derivative of 8325-4) and in one clinical isolate.