ArticleCommunications biology2025
(p)ppGpp-mediated GTP homeostasis ensures survival and antibiotic tolerance of Staphylococcus aureus.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Bacterial growth rate in populations and single cells.Nature microbiology · 2026Review
- RelA-mediated (p)ppGpp accumulation links glucose starvation to peptidoglycan synthesis arrest and spherical morphogenesis via PBP2x and FtsX inJournal of bacteriology · 2026Article
- Network-based bioinformatics for the prediction of candidate SNPs in Staphylococcus aureus virulence and resistance genes.Folia microbiologica · 2026Article
- Sustained ppGpp production underpins months-long survival of a bacterium in growth arrest.mBio · 2026Article
- Targeting the stringent response alters gene expression and extracellular vesicle RNA inMicrobiology spectrum · 2026Article
- Non-canonical stringent response signaling mediates antimicrobial fatty acid sensitivity inbioRxiv : the preprint server for biology · 2026Article
- Flipping the magic switch to persistence via GTP depletion.Nature microbiology · 2025Article
- Article
- Integrated genomic and proteomic analysis of the mouse-adaptedCurrent research in microbial sciences · 2025Article
- Prokaryotic homeostasis - a solution to thrive and survive.Frontiers in molecular biosciences · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Antibiotic tolerance in non-growing bacterial populations is of major concern regarding antibiotic treatment failures. Whether and how the messenger molecule (p)ppGpp contributes to this phenomenon is controversial. We show for Staphylococcus aureus that (p)ppGpp-dependent restriction of the GTP pool is essential for the culturability of starved cells. Survival was independent of the GTP-responsive regulator CodY. Elevated GTP levels in a starved (p)ppGpp-deficient mutant led to quiescent state characterised by alterations in membrane architecture and a decrease of the proton motive force (PMF). This was accompanied by dysregulation of components involved in electron transport, including qoxABCD, encoding the main terminal oxidase. Increasing qoxABCD transcription by mutation of the transcription start site (iATP to iGTP) partially restored the culturability of the (p)ppGpp-deficient mutant. Thus, regulation of nucleotide-dependent promoters by altered nucleotide levels contribute to starvation adaptability. Loss of PMF under high GTP conditions also renders bacteria susceptible to antibiotics. Thus, targeting the PMF or nucleotide availability may be a valuable strategy to combat antibiotic tolerance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.