The Staphylococcus-Specific Gene rsr Represses agr and Virulence in Staphylococcus aureus

被引：13

作者：

Tamber, Sandeep ^{[1
]}

Reyes, Dindo ^{[1
]}

Donegan, Niles P. ^{[1
]}

Schwartzman, Joseph D. ^{[2
]}

Cheung, Ambrose L. ^{[1
]}

Memmi, Guido ^{[1
]}

机构：

[1] Dartmouth Med Sch, Dept Microbiol & Immunol, Hanover, NH 03755 USA

[2] Dartmouth Hitchcock Med Ctr, Microbiol Sect, Dept Pathol, Lebanon, NH 03756 USA

来源：

INFECTION AND IMMUNITY | 2010年 / 78卷 / 10期

关键词：

PATHOGENICITY ISLANDS; EXPRESSION; IDENTIFICATION; REGULATOR; STRAIN; SARA; DETERMINANTS; RESISTANCE; EVOLUTION; SEQUENCE;

D O I：

10.1128/IAI.00401-10

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The expression of virulence factors in Staphylococcus aureus is tightly coordinated by a vast network of regulatory molecules. In this report, we characterize a genetic locus unique to staphylococci called rsr that has a role in repressing two key virulence regulators, sarR and agr. Using strain SH1000, we showed that the transcription of virulence effectors, such as hla, sspA, and spa, is altered in an rsr mutant in a way consistent with agr upregulation. Analysis of RNAIII expression of the agr locus in rsr and rsr-sarR mutants indicated that rsr likely contributes to agr expression independently of SarR. We also provide evidence using a murine model of S. aureus skin infection that the effects mediated by rsr reduce disease progression.

引用

页码：4384 / 4391

页数：8

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