Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA679480 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13084817_1.fastq.gz	Fastqsanger.gz
	SRR13084817_2.fastq.gz	Fastqsanger.gz
	SRR13084818_1.fastq.gz	Fastqsanger.gz
	SRR13084818_2.fastq.gz	Fastqsanger.gz
	SRR13084819_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

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

| PRJNA679298 | ENA

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

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

| PRJNA679299 | ENA

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]

| PRJNA679481 | ENA

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]

| PRJNA679302 | ENA

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

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.

2021-06-01 | GSE161755 | GEO