ArticleMolecular microbiology2016
The LysR-type transcriptional regulator, CidR, regulates stationary phase cell death in Staphylococcus aureus.
Article in Molecular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
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- Targeting the Holy Triangle of Quorum Sensing, Biofilm Formation, and Antibiotic Resistance in Pathogenic Bacteria.Microorganisms · 2022Review
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- Staphylococcal ClpXP protease targets the cellular antioxidant system to eliminate fitness-compromised cells in stationary phase.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Extracellular DNA released by glycine-auxotrophic Staphylococcus epidermidis small colony variant facilitates catheter-related infections.Communications biology · 2021Article
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- Transcriptomic Analysis ofMicroorganisms · 2020Article
- The acid response network of Staphylococcus aureus.Current opinion in microbiology · 2020Review
- Acetate and Potassium Modulate the Stationary-Phase Activation ofFrontiers in microbiology · 2020Article
- CidR and CcpA Synergistically Regulate Staphylococcus aureusJournal of bacteriology · 2019Article
- Characterization of LrgAB as a stationary phase-specific pyruvate uptake system in Streptococcus mutans.BMC microbiology · 2019Article
- An unconventional RNA-based thermosensor within the 5' UTR of Staphylococcus aureus cidA.PloS one · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
The Staphylococcus aureus LysR-type transcriptional regulator, CidR, activates the expression of two operons including cidABC and alsSD that display pro- and anti-death functions, respectively. Although several investigations have focused on the functions of different genes associated with these operons, the collective role of the CidR regulon in staphylococcal physiology is not clearly understood. Here we reveal that the primary role of this regulon is to limit acetate-dependent potentiation of cell death in staphylococcal populations. Although both CidB and CidC promote acetate generation and cell death, the CidR-dependent co-activation of CidA and AlsSD counters the effects of CidBC by redirecting intracellular carbon flux towards acetoin formation. From a mechanistic standpoint, we demonstrate that CidB is necessary for full activation of CidC, whereas CidA limits the abundance of CidC in the cell.
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