期刊
SCIENCE
卷 354, 期 6318, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf4268
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资金
- Danish National Research Foundation-funded Centre of Excellence BASP [DNRF120]
- Novo Nordisk Foundation Laureate Research grant
- European Research Council Advanced Investigator grant PERSIST [294517]
- European Molecular Biology Organization Long-Term Fellowship [ALTF 564-2016]
Bacterial persister cells avoid antibiotic-induced death by entering a physiologically dormant state and are considered a major cause of antibiotic treatment failure and relapsing infections. Such dormant cells form stochastically, but also in response to environmental cues, by various pathways that are usually controlled by the second messenger (p)ppGpp. For example, toxin-antitoxin modules have been shown to play a major role in persister formation in many model systems. More generally, the diversity of molecular mechanisms driving persister formation is increasingly recognized as the cause of physiological heterogeneity that underlies collective multistress and multidrug tolerance of persister subpopulations. In this Review, we summarize the current state of the field and highlight recent findings, with a focus on the molecular basis of persister formation and heterogeneity.
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