ArticlePloS one2011
A toxin-antitoxin module in Bacillus subtilis can both mitigate and amplify effects of lethal stress.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Quorum-sensingeLife · 2024Article
- Quorum-sensingbioRxiv : the preprint server for biology · 2024Article
- Arbitrium communication controls phage lysogeny through non-lethal modulation of a host toxin-antitoxin defence system.Nature microbiology · 2024Article
- Quinolone Antibiotics: Resistance and Therapy.Infection and drug resistance · 2023Review
- Fluoroquinolone heteroresistance, antimicrobial tolerance, and lethality enhancement.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Genomic analysis of Caldalkalibacillus thermarum TA2.A1 reveals aerobic alkaliphilic metabolism and evolutionary hallmarks linking alkaliphilic bacteria and plant life.Extremophiles : life under extreme conditions · 2020Article
- Toxin⁻Antitoxin Systems inToxins · 2019Review
- Suppression of Reactive Oxygen Species Accumulation Accounts for Paradoxical Bacterial Survival at High Quinolone Concentration.Antimicrobial agents and chemotherapy · 2018Article
- Desperate times call for desperate measures: benefits and costs of toxin-antitoxin systems.Current genetics · 2017Review
- Toxin ζ Triggers a Survival Response to Cope with Stress and Persistence.Frontiers in microbiology · 2017Article
- Comparative Genomics ofFrontiers in microbiology · 2017Article
- Mycobacteriophage SWU1 gp39 can potentiate multiple antibiotics against Mycobacterium via altering the cell wall permeability.Scientific reports · 2016Article
- Moving forward with reactive oxygen species involvement in antimicrobial lethality.The Journal of antimicrobial chemotherapy · 2015Review
- Article
- Reactive oxygen species and the bacterial response to lethal stress.Current opinion in microbiology · 2014Review
- Article
- Superoxide-mediated protection of Escherichia coli from antimicrobials.Antimicrobial agents and chemotherapy · 2013Article
- YihE kinase is a central regulator of programmed cell death in bacteria.Cell reports · 2013Article
- Localized cell death focuses mechanical forces during 3D patterning in a biofilm.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundBacterial type-2 (protein-protein) toxin-antitoxin (TA) modules are two-gene operons that are thought to participate in the response to stress. Previous work with Escherichia coli has led to a debate in which some investigators conclude that the modules protect from stress, while others argue that they amplify lethal stress and lead to programmed cell death. To avoid ambiguity arising from the presence of multiple TA modules in E. coli, the effect of the sole type-2 toxin-antitoxin module of Bacillus subtilis was examined for several types of lethal stress. METHODOLOGY/PRINCIPAL
findingsGenetic knockout of the toxin gene, ndoA (ydcE), conferred protection to lethal stressors that included kanamycin, moxifloxacin, hydrogen peroxide, and UV irradiation. However, at low doses of UV irradiation the ndoA deficiency increased lethality. Indeed, gradually increasing UV dose with the ndoA mutant revealed a crossover response--from the mutant being more sensitive than wild-type cells to being less sensitive. For high temperature and nutrient starvation, the toxin deficiency rendered cells hypersensitive. The ndoA deficiency also reduced sporulation frequency, indicating a role for toxin-antitoxin modules in this developmental process. In the case of lethal antimicrobial treatment, deletion of the toxin eliminated a surge in hydrogen peroxide accumulation observed in wild-type cells.
conclusionsA single toxin-antitoxin module can mediate two opposing effects of stress, one that lowers lethality and another that raises it. Protective effects are thought to arise from toxin-mediated inhibition of translation based on published work. The enhanced, stress-mediated killing probably involves toxin-dependent accumulation of reactive oxygen species, since a deficiency in the NdoA toxin suppressed peroxide accumulation following antimicrobial treatment. The type and perhaps the level of stress appear to be important for determining whether this toxin will have a protective or detrimental effect.
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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.