Characterization of a sar homolog of Staphylococcus epidermidis.

Coagulase-negative staphylococci are common nosocomial pathogens. A regulatory element, designated sar, partially controls exoprotein synthesis in coagulase-positive Staphylococcus aureus by modulating the expression of another regulatory locus, called agr. We report here the cloning of a sar homolog in S. epidermidis. The major open reading frame within sar in S. epidermidis is highly homologous (84%) to the S. aureus SarA protein. Primer extension studies revealed three sar transcripts (0.64, 0.76, and 0.85 kb) initiated from three distinct promoters. The interpromoter region in S. epidermidis differs from its S. aureus counterpart, possibly suggesting target gene differences and a disparate pattern for sar activation. Remarkably, the S. epidermidis sar homolog interacts with an agr promoter fragment of S. aureus in gel shift assays. Additionally, S. epidermidis sar fragments could restore hemolysin production in an S. aureus sar mutant. As typical virulence determinants controlled by sar in S. aureus are not present in S. epidermidis, an examination of functional and structural similarities and divergence of sar in staphylococci will be of major interest.