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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T4infection_RNAseq]

ABSTRACT: The purpose of this experiment was to characterize ToxN activity following T4 infection.

ORGANISM(S): Escherichia coli str. K-12 substr. MG1655

PROVIDER: GSE161794 | GEO | 2021/06/01

REPOSITORIES: GEO

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T7infection_RNAseq]

Project description:The purpose of this experiment was to characterize ToxN activity following T7 infection.

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_riftreatment_RNAseq]

Project description:The purpose of this experiment was to characterize ToxN activity following activation by rifampicin treatment.

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxN_overexpression_RNAseq]

Project description:The purpose of this experiment was to characterize ToxN cleavage specificity and locations of cleavage genome-wide in E. coli following overexpression.

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection.

Project description: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.

| S-EPMC8284924 | biostudies-literature

Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-01 | GSE161756 | GEO

A phage-encoded RNA-binding protein inhibits the antiviral activity of a toxin-antitoxin system

Project description:Bacteria harbor diverse mechanisms to defend themselves against their viral predators, bacteriophages. In response, phages can evolve counter-defense systems, most of which remain poorly understood. In T4-like phages, the gene tifA prevents bacterial defense by the type III toxin-antitoxin (TA) system toxIN, but the mechanism by which TifA inhibits toxIN remains unclear. Here, we show that TifA directly binds both the endoribonuclease ToxN and RNA, leading to the formation of a high molecular weight ribonucleoprotein complex in which ToxN is inhibited. The RNA binding activity of TifA is necessary for its interaction with and inhibition of ToxN. Thus, we propose that TifA inhibits ToxN during phage infection by trapping ToxN on cellular RNA, particularly the abundant 16S rRNA, preventing cleavage of phage transcripts. Taken together, our results reveal a novel mechanism underlying inhibition of a phage-defensive RNase toxin by a small, phage-encoded protein.

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection

Project description:Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T4infection_RNAseq]

Project description:Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T4infection_RNAseq]

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxN_overexpression_RNAseq]

Project description:Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxN_overexpression_RNAseq]

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Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T7infection_RNAseq]

Project description:Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection [toxIN_T7infection_RNAseq]

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