Coagulase-negative staphylococci are common nosocomial pathogens. A re
gulatory element, designated sar, partially controls exoprotein synthe
sis in coagulase-positive Staphylococcus aureus by modulating the expr
ession of another regulatory locus, called agr. We report here the clo
ning of a sar homolog in S. epidermidis. The major open reading frame
within sar in S. epidermidis is highly homologous (84%) to the S. aure
us SarA protein. Primer extension studies revealed three sar transcrip
ts (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 dispara
te pattern for sar activation. Remarkably, the S. epidermidis sar homo
log interacts with an agr promoter fragment of S. aureus in gel shift
assays. Additionally, S. epidermidis sar fragments could restore hemol
ysin production in an S. aureus sar mutant. As typical virulence deter
minants controlled by sar in S. aureus are not present in S. epidermid
is, an examination of functional and structural similarities and diver
gence of sar in staphylococci will be of major interest.