About this item:

505 Views | 0 Downloads

Author Notes:

Corresponding author: Gordon Churchward, Department of Microbiology and Immunology, Emory University School of Medicine, 1510 Clifton Road, Atlanta, GA 30345, Tel: 404 727 2538, Fax: 404 727 3659, gordon.churchward@emory.edu

Current address: Laboratories of Microbial Pathogenesis, VA Medical Center, Decatur, Georgia 30033

Subjects:

Research Funding:

This work was supported by grant AI020723 from NIH. C.B. was supported in part by IRACDA NIH/NIGMS grant K12 GM000680 to Emory University and the Atlanta University Center.

A.A.G. was supported in part by NIH training grant T32 AI07470 and by a UNCF-Merck Graduate Science Research Dissertation Fellowship.

Regulation of streptokinase expression by CovR/S in Streptococcus pyogenes: CovR acts through a single high affinity binding site

Tools:

Journal Title:

Microbiology

Volume:

Volume 155, Number 0 2

Publisher:

, Pages 566-575

Type of Work:

Article | Post-print: After Peer Review

Abstract:

SUMMARY The important human pathogen Streptococcus pyogenes (the group A streptococcus or GAS) produces many virulence factors that are regulated by the two-component signal transduction system CovRS (CsrRS). Dissemination of GAS infection originating at the skin has been shown to require production of streptokinase, whose transcription is repressed by CovR. In this work we have studied the interaction of CovR and phosphorylated CovR (CovR-P) with the promoter for streptokinase, Pska. We found that, in contrast to the other CovR-repressed promoters, Pska regulation by CovR occurs through binding at a single ATTARA consensus binding sequence (CB) that overlaps the −10 region of the promoter. Binding of CovR to other nearby consensus sequences occurs upon phosphorylation of the protein, but these other CBs do not contribute to the regulation of Pska by CovR. Thus, binding at a specific site does not necessarily indicate that site is involved in regulation by CovR. In addition, at Pska, CovR binding to the different sites does not appear to involve cooperative interactions, which simplifies the analysis of CovR binding and gives us insight into the modes of interaction that occur between CovR and its specific DNA binding sites. Finally, the observation that regulation of transcription from Pska occurs at a very low concentration of phosphorylated CovR may have important implications for the regulation of virulence gene expression during group A streptococcal infection.

Copyright information:

© 2014 Society for General Microbiology

Export to EndNote