ArticleNature microbiology2016
Growth control switch by a DNA-damage-inducible toxin-antitoxin system in Caulobacter crescentus.
Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- An ancestral transmembrane transcription factor couples cell envelope regulation and the SOS response in Caulobacter crescentus.PLoS genetics · 2026Article
- Asymmetric envelope surface disposition of secreted protein YjbI controls bimodal antibiotic susceptibilities in C. crescentus.The EMBO journal · 2026Article
- Variability in intrinsic promoter strength underlies the temporal hierarchy of the Caulobacter SOS response induction.PLoS biology · 2025Article
- A delivered DNase toxin creates population heterogeneity through transient intoxication of siblings.mBio · 2025Article
- Contribution of Toxin-Antitoxin Systems to Adherent-InvasiveMicroorganisms · 2024Review
- Adaptive β-lactam resistance from an inducible efflux pump that is post-translationally regulated by the DjlA co-chaperone.PLoS biology · 2023Article
- eDNA-stimulated cell dispersion fromeLife · 2023Article
- Substrate recognition and cryo-EM structure of the ribosome-bound TAC toxin of Mycobacterium tuberculosis.Nature communications · 2022Article
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- ThemSphere · 2021Article
- Biological Functions of Type II Toxin-Antitoxin Systems in Bacteria.Microorganisms · 2021Review
- Insights into the global effect on Staphylococcus aureus growth arrest by induction of the endoribonuclease MazF toxin.Nucleic acids research · 2020Article
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- Structural basis of transcriptional regulation by the HigA antitoxin.Molecular microbiology · 2019Article
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- Iron Deficiency Generates Oxidative Stress and Activation of the SOS Response inFrontiers in microbiology · 2018Article
- Artificial Activation ofFrontiers in microbiology · 2018Article
- TSS-EMOTE, a refined protocol for a more complete and less biased global mapping of transcription start sites in bacterial pathogens.BMC genomics · 2016Article
- The MqsRA Toxin-Antitoxin System from Xylella fastidiosa Plays a Key Role in Bacterial Fitness, Pathogenicity, and Persister Cell Formation.Frontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial toxin-antitoxin systems (TASs) are thought to respond to various stresses, often inducing growth-arrested (persistent) sub-populations of cells whose housekeeping functions are inhibited. Many such TASs induce this effect through the translation-dependent RNA cleavage (RNase) activity of their toxins, which are held in check by their cognate antitoxins in the absence of stress. However, it is not always clear whether specific mRNA targets of orthologous RNase toxins are responsible for their phenotypic effect, which has made it difficult to accurately place the multitude of TASs within cellular and adaptive regulatory networks. Here, we show that the TAS HigBA of Caulobacter crescentus can promote and inhibit bacterial growth dependent on the dosage of HigB, a toxin regulated by the DNA damage (SOS) repressor LexA in addition to its antitoxin HigA, and the target selectivity of HigB's mRNA cleavage activity. HigB reduced the expression of an efflux pump that is toxic to a polarity control mutant, cripples the growth of cells lacking LexA, and targets the cell cycle circuitry. Thus, TASs can have outcome switching activity in bacterial adaptive (stress) and systemic (cell cycle) networks.
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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.