Linked Life Data

18681938

Source:http://linkedlifedata.com/resource/pubmed/id/18681938

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pubmed-article:18681938pubmed:abstractTextStreptococcus mutans is a primary pathogen for dental caries in humans. CiaR and CiaH of S. mutans comprise a two-component signal transduction system (TCS) involved in regulating various virulent factors. However, the signal that triggers the CiaRH response remains unknown. In this study, we show that calcium is a signal for regulation of the ciaRH operon, and that a double-glycine-containing small peptide encoded within the ciaRH operon (renamed ciaX) mediates this regulation. CiaX contains a serine + aspartate (SD) domain that is shared by calcium-binding proteins. A markerless in-frame deletion of ciaX reduced ciaRH operon expression and diminished the calcium repression of operon transcription. Point mutations of the SD domain resulted in the same phenotype as the in-frame deletion, indicating that the SD domain is required for CiaX function. Further characterization of ciaX demonstrated that it is involved in calcium-mediated biofilm formation. Furthermore, inactivation of ciaR or ciaH led to the same phenotype as the in-frame deletion of ciaX, suggesting that all three genes are involved in the same regulatory pathway. Sequence analysis and real-time RT-PCR identified a putative CiaR binding site upstream of ciaX. We conclude that the ciaXRH operon is a three-component, self-regulatory system modulating cellular functions in response to calcium.lld:pubmed
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pubmed-article:18681938pubmed:dateRevised2011-9-26lld:pubmed
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pubmed-article:18681938pubmed:year2008lld:pubmed
pubmed-article:18681938pubmed:articleTitleThe cia operon of Streptococcus mutans encodes a unique component required for calcium-mediated autoregulation.lld:pubmed
pubmed-article:18681938pubmed:affiliationUCLA School of Dentistry, Los Angeles, CA 90095, USA.lld:pubmed
pubmed-article:18681938pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18681938pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:18681938pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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