JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow An authors' corrections has been published
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rolerson, E.
Right arrow Articles by Spatafora, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rolerson, E.
Right arrow Articles by Spatafora, G.
Journal of Bacteriology, July 2006, p. 5033-5044, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00155-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The SloR/Dlg Metalloregulator Modulates Streptococcus mutans Virulence Gene Expression

Elizabeth Rolerson, Adam Swick, Lindsay Newlon, Cameron Palmer, Yong Pan, Britton Keeshan, and Grace Spatafora*

Department of Biology, Middlebury College, 276 Bicentennial Way, MBH354, Middlebury, Vermont 05753

Received 27 January 2006/ Accepted 17 April 2006

Metal ion availability in the human oral cavity plays a putative role in Streptococcus mutans virulence gene expression and in appropriate formation of the plaque biofilm. In this report, we present evidence that supports such a role for the DtxR-like SloR metalloregulator (called Dlg in our previous publications) in this oral pathogen. Specifically, the results of gel mobility shift assays revealed the sloABC, sloR, comDE, ropA, sod, and spaP promoters as targets of SloR binding. We confirmed differential expression of these genes in a GMS584 SloR-deficient mutant versus the UA159 wild-type progenitor by real-time semiquantitative reverse transcriptase PCR experiments. The results of additional expression studies support a role for SloR in S. mutans control of glucosyltransferases, glucan binding proteins, and genes relevant to antibiotic resistance. Phenotypic analysis of GMS584 revealed that it forms aberrant biofilms on an abiotic surface, is compromised for genetic competence, and demonstrates heightened incorporation of iron and manganese as well as resistance to oxidative stress compared to the wild type. Taken together, these findings support a role for SloR in S. mutans adherence, biofilm formation, genetic competence, metal ion homeostasis, oxidative stress tolerance, and antibiotic gene regulation, all of which contribute to S. mutans-induced disease.


* Corresponding author. Mailing address: Department of Biology, Middlebury College, 276 Bicentennial Way, MBH354, Middlebury, Vermont 05753. Phone: (802) 443-5431. Fax: (802) 443-2072. E-mail: spatafor{at}middlebury.edu.


Journal of Bacteriology, July 2006, p. 5033-5044, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00155-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2006 by the American Society for Microbiology. All rights reserved.