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Journal of Bacteriology, January 2008, p. 28-36, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.01395-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of RelA of Streptococcus mutans in Global Control of Gene Expression{triangledown} ,{dagger}

Marcelle M. Nascimento, José A. Lemos,{ddagger} Jacqueline Abranches,{ddagger} Vanessa K. Lin, and Robert A. Burne*

Department of Oral Biology, University of Florida College of Dentistry, Gainesville, Florida 32610

Received 28 August 2007/ Accepted 9 October 2007

The production of (p)ppGpp by Streptococcus mutans UA159 is catalyzed by three gene products: RelA, RelP, and RelQ. Here, we investigate the role of the RelA (Rel) homologue of S. mutans in the stringent response and in the global control of gene expression. RelA of S. mutans was shown to synthesize pppGpp in vitro from GTP and ATP in the absence of added ribosomes, as well as in vivo in an Escherichia coli relA-spoT mutant. Mupirocin (MUP) was shown to induce high levels of (p)ppGpp production in S. mutans in a relA-dependent manner, with a concomitant reduction in GTP pools. Transcription profiling after MUP treatment of S. mutans revealed that 104 genes were upregulated and 130 were downregulated (P ≤ 0.001); mainly, genes for macromolecular biosynthesis, translation, and energy metabolism were downregulated. When a derivative of UA159 carrying a complete deletion of the relA gene was treated with MUP, 72 genes were upregulated and 52 were downregulated (P ≤ 0.001). The expression of 50 genes (P ≤ 0.001) was commonly affected by MUP treatment in the two strains, suggesting that S. mutans can mount a relA-independent response to MUP. Consistent with the gene expression profiling, RelA was shown to play major roles in the regulation of phenotypic traits that are required for establishment, persistence, and virulence expression by this oral pathogen. Thus, RelA is the major (p)ppGpp synthase controlling the stringent response in S. mutans, and it coordinates the expression of genes and phenotypes that contribute to the pathogenic potential of the organism.

* Corresponding author. Mailing address: Department of Oral Biology, University of Florida College of Dentistry, Gainesville, FL 32610. Phone: (352) 392-4370. Fax: (352) 392-7357. E-mail: rburne{at}dental.ufl.edu

{triangledown} Published ahead of print on 19 October 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} Present address: Center for Oral Biology, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642.

Journal of Bacteriology, January 2008, p. 28-36, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.01395-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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