ArticleMolecular cell2021
Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 122 citations in OpenAlex.
- How bacterial immune systems sense phage infection.Nature reviews. Microbiology · 2026Review
- Revisiting the life cycle of temperate phages.Nature reviews. Microbiology · 2026Review
- The PhageExpressionAtlas reveals shared and unique transcriptional patterns across phage-host interactions.NAR genomics and bioinformatics · 2026Article
- Review
- Phage host range: determinants, dynamics and applications.Nature reviews. Microbiology · 2026Review
- Rapid and quantitative measurement of bacteriophage infectivity via fully automated droplet digital PCR.Nature communications · 2026Article
- Potential role of a CRISPR-Cas-activated toxin-antitoxin system in bacterial immunity.Nature communications · 2026Article
- Ribosomal RNA cleavage by the previously unidentified RelS-RelI toxin-antitoxin system controls growth of Mycobacterium tuberculosis.Nucleic acids research · 2026Article
- A bacterial CARD-NLR-like immune system controls the release of gene transfer agents.Nature microbiology · 2026Article
- DefensePredictor: A machine learning model to discover prokaryotic immune systems.Science (New York, N.Y.) · 2026Article
- Article
- The molecular mechanisms of the ShosTA system in mediating anti-phage defense.Nucleic acids research · 2026Article
- Bacterial defense mechanisms against bacteriophages: an evolutionary arms race.Archives of microbiology · 2026Review
- Revisiting lactococcal abortive infection-like antiphage systems: diversity, structures, and mechanisms.FEMS microbiology reviews · 2026Review
- Re-evaluating the role ofmicroPublication biology · 2026Article
- Post-transcriptional control during T4 infection.EcoSal Plus · 2025Review
- Design of orthogonal and portable RNA devices for post-transcriptional regulation by reverse engineering type I toxin-antitoxin systems.Nucleic acids research · 2025Article
- Phage nuclease-mediated defense activation of the bacterial Retron-Eco7 toxin-antitoxin system.Nucleic acids research · 2025Article
- Battle beyond membrane: flagella as a conduit for phage DNA entry and a trigger for bacterial defense in Yersinia enterocolitica.Nucleic acids research · 2025Article
- Ribonuclease toxin RelE1 inhibits growth of Mycobacterium tuberculosis through specific cleavage of the ribosomal anti-Shine-Dalgarno region.Nucleic acids research · 2025Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Toxin-antitoxin (TA) systems are widespread in bacteria, but their activation mechanisms and bona fide targets remain largely unknown. Here, we characterize a type III TA system, toxIN, that protects E. coli against multiple bacteriophages, including T4. Using RNA sequencing, we find that the endoribonuclease ToxN is activated following T4 infection and blocks phage development primarily by cleaving viral mRNAs and inhibiting their translation. ToxN activation arises from T4-induced shutoff of host transcription, specifically of toxIN, leading to loss of the intrinsically unstable toxI antitoxin. Transcriptional shutoff is necessary and sufficient for ToxN activation. Notably, toxIN does not strongly protect against another phage, T7, which incompletely blocks host transcription. Thus, our results reveal a critical trade-off in blocking host transcription: it helps phage commandeer host resources but can activate potent defense systems. More generally, our results now reveal the native targets of an RNase toxin and activation mechanism of a phage-defensive TA system.
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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.