Journal article
The CsoR-like sulfurtransferase repressor (CstR) is a persulfide sensor in Staphylococcus aureus
Molecular microbiology, Vol.94(6), pp.1343-1360
12/2014
DOI: 10.1111/mmi.12835
PMCID: PMC4264537
PMID: 25318663
Abstract
How cells regulate the bioavailability of utilizable sulfur while mitigating the effects of hydrogen sulfide toxicity is poorly understood. CstR [Copper-sensing operon repressor (CsoR)-like sulfurtransferase repressor] represses the expression of the cst operon encoding a putative sulfide oxidation system in Staphylococcus aureus. Here, we show that the cst operon is strongly and transiently induced by cellular sulfide stress in an acute phase and specific response and that cst-encoded genes are necessary to mitigate the effects of sulfide toxicity. Growth defects are most pronounced when S. aureus is cultured in chemically defined media with thiosulfate (TS) as a sole sulfur source, but are also apparent when cystine is used or in rich media. Under TS growth conditions, cells fail to grow as a result of either unregulated expression of the cst operon in a Delta cstR strain or transformation with a non-inducible C31A/C60A CstR that blocks cst induction. This suggests that the cst operon contributes to cellular sulfide homeostasis. Tandem high-resolution mass spectrometry reveals derivatization of CstR by both inorganic tetrasulfide and an organic persulfide, glutathione persulfide, to yield a mixture of Cys31-Cys60' interprotomer cross-links, including di-, tri- and tetrasulfide bonds, which allosterically inhibit cst operator DNA binding by CstR.
Details
- Title: Subtitle
- The CsoR-like sulfurtransferase repressor (CstR) is a persulfide sensor in Staphylococcus aureus
- Creators
- Justin L. Luebke - Indiana University BloomingtonJiangchuan Shen - Indiana UniversityKevin E. Bruce - Indiana University BloomingtonThomas E. Kehl-Fie - University of Illinois Urbana-ChampaignHui Peng - Indiana University BloomingtonEric P. Skaar - Vanderbilt UniversityDavid P. Giedroc - Indiana University Bloomington
- Resource Type
- Journal article
- Publication Details
- Molecular microbiology, Vol.94(6), pp.1343-1360
- DOI
- 10.1111/mmi.12835
- PMID
- 25318663
- PMCID
- PMC4264537
- NLM abbreviation
- Mol Microbiol
- ISSN
- 0950-382X
- eISSN
- 1365-2958
- Publisher
- Wiley
- Number of pages
- 18
- Grant note
- R01 GM097225; R01 AI069233 / US National Institutes of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA F32 AI100480; K22 AI104805 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA R01GM097225 / NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of General Medical Sciences (NIGMS) F32AI100480 / NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID)
- Language
- English
- Date published
- 12/2014
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984618524502771
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