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Infection and Immunity, February 2002, p. 762-770, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.762-770.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Rgg Influences the Expression of Multiple Regulatory Loci To Coregulate Virulence Factor Expression in Streptococcus pyogenes

Michael S. Chaussee,* Gail L. Sylva, Daniel E. Sturdevant, Laura M. Smoot, Morag R. Graham, Robert O. Watson, and James M. Musser

Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840,

Received 15 August 2001/ Returned for modification 8 October 2001/ Accepted 22 October 2001

The human pathogen Streptococcus pyogenes secretes many proteins to the cell wall and extracellular environment that contribute to virulence. Rgg regulates the expression of several exoproteins including a cysteine protease (SPE B), a nuclease (MF-1), a putative nuclease (MF-3), and autolysin. The functional heterogeneity of Rgg-regulated exoproteins and the lack of a conserved regulatory motif in the promoter regions of the genes suggested that Rgg interacts with additional regulatory networks to influence gene expression. DNA microarrays were used to test this hypothesis by comparing genomewide transcript profiles of S. pyogenes NZ131 and isogenic derivative NZ131 rgg during the exponential phase of growth. Transcripts of known and putative virulence-associated genes were more abundant in the rgg mutant, including emm, scpA, orfX, scl1, hasAB, slo, sagA, ska, speH, grab, mac, mf-1, and mf-3. Increased transcription of emm, scpA, and orfX in the rgg mutant was associated with increased production of the corresponding proteins. Differences in the expression of virulence-associated genes were associated with changes in the expression of several regulatory genes, including mga, sagA, csrRS, and fasBCA. The results show that Rgg influences the expression of multiple regulatory networks to coregulate virulence factor expression in S. pyogenes.

* Corresponding author. Mailing address: Division of Basic Biomedical Sciences, College of Medicine, University of South Dakota, Lee Medical Building, 414 East Clark St., Vermillion, SD 57069-2390. Phone: (605) 677-6681. Fax: (605) 677-6381. E-mail: mchausse{at}0040usd.edu.

Editor: E. I. Tuomanen

{dagger} Present address: Section of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536

Infection and Immunity, February 2002, p. 762-770, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.762-770.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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