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Infection and Immunity, January 2003, p. 343-353, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.343-353.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

sarU, a sarA Homolog, Is Repressed by SarT and Regulates Virulence Genes in Staphylococcus aureus

Adhar C. Manna* and Ambrose L. Cheung

Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 03755

Received 29 August 2002/ Returned for modification 3 October 2002/ Accepted 11 October 2002

In searching the Staphylococcus aureus genome, we previously identified sarT, a homolog of sarA, which encodes a repressor for {alpha}-hemolysin synthesis. Adjacent but transcribed divergently to sarT is sarU, which encodes a 247-residue polypeptide, almost twice the length of SarA. Sequence alignment disclosed that SarU, like SarS, which is another SarA homolog, could be envisioned as a molecule with two halves, with each half being homologous to SarA. SarU, as a member of the SarA family proteins, disclosed conservation of basic residues within the helix-turn-helix motif and within the beta hairpin loop, two putative DNA binding domains within this protein family. The transcription of sarU is increased in a sarT mutant. Gel shift and transcriptional fusion studies revealed that SarT can bind to the sarU promoter region, probably acting as a repressor for sarU transcription. The expression of RNAII and RNAIII of agr is decreased in a sarU mutant. As RNAIII expression is up-regulated in a sarT mutant, we hypothesize that sarT may down regulate agr RNAIII expression by repressing sarU, a positive activator of agr expression. We propose that, in addition to the quorum sensing effect of the autoinducing peptide of agr, the sarT-sarU pathway may represent a secondary amplification loop whereby the expression of agr (e.g., those found in vivo) might repress sarT, leading to increased expression of sarU. Elevated sarU expression would result in additional amplification of the original agr signal.

* Corresponding author. Mailing address: Vail 206, Department of Microbiology, Dartmouth Medical School, Hanover, NH 03755. Phone: (630) 650-1310. Fax: (603) 650-1362. E-mail: Adhar.C.Manna{at}Dartmouth.EDU.

Editor: A. D. O'Brien

Infection and Immunity, January 2003, p. 343-353, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.343-353.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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