Document Detail


SloR modulation of the Streptococcus mutans acid tolerance response involves the GcrR response regulator as an essential intermediary.
MedLine Citation:
PMID:  18375805     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Streptococcus mutans, the primary causative agent of human dental caries, grows as a biofilm on the tooth surface, where it metabolizes dietary carbohydrates and generates acid byproducts that demineralize tooth enamel. A drop in plaque pH stimulates an adaptive acid-tolerance response (ATR) in this oral pathogen that allows it to survive acid challenge at pHs as low as 3.0. In the present study, we describe the growth of an S. mutans mutant, GMS901, that harbours an insertion-deletion mutation in gcrR, a gene that encodes a transcriptional regulatory protein. The mutant is acid-sensitive and significantly compromised in its ATR relative to the UA159 wild-type progenitor strain. Consistent with these findings are the results of real-time quantitative RT-PCR (qRT-PCR) experiments that support the GcrR-regulated expression of known ATR genes, including atpA/E and ffh. Although we observed gcrR transcription that was not responsive to acidic pH, we did note a significant increase in gcrR expression when S. mutans cells were grown in a manganese-restricted medium. Interestingly, the results of gel mobility shift assays indicate that the S. mutans SloR metalloregulatory protein is a potential regulator of gcrR by virtue of its manganese-dependent binding to the gcrR promoter region, and expression studies support the hypothesis that sloR transcription is responsive to manganese deprivation and acidic pH. Taking these results together, we propose that SloR-Mn modulates S. mutans gcrR expression as part of a general stress response, and that GcrR acts downstream of SloR to control the ATR.
Authors:
Daniel W Dunning; Lathan W McCall; William F Powell; W Tristram Arscott; Erin M McConocha; Cheryl J McClurg; Steven D Goodman; Grace A Spatafora
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Microbiology (Reading, England)     Volume:  154     ISSN:  1350-0872     ISO Abbreviation:  Microbiology (Reading, Engl.)     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-31     Completed Date:  2008-06-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9430468     Medline TA:  Microbiology     Country:  England    
Other Details:
Languages:  eng     Pagination:  1132-43     Citation Subset:  IM    
Affiliation:
Department of Biology, Middlebury College, Middlebury, VT 05753, USA.
Data Bank Information
Bank Name/Acc. No.:
GEO/GSE10215
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MeSH Terms
Descriptor/Qualifier:
Acids / metabolism*
Bacterial Proteins / genetics,  physiology*
DNA, Bacterial / metabolism
Electrophoretic Mobility Shift Assay
Gene Expression Profiling
Gene Order
Humans
INDEL Mutation
Manganese / metabolism
Microbial Viability
Protein Binding
Reverse Transcriptase Polymerase Chain Reaction
Streptococcus mutans / drug effects,  physiology*
Transcription Factors / genetics,  physiology*
Grant Support
ID/Acronym/Agency:
P20 RR 16462/RR/NCRR NIH HHS; R01 DE 014711/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Acids; 0/Bacterial Proteins; 0/DNA, Bacterial; 0/Transcription Factors; 7439-96-5/Manganese

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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