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The phage abortive infection system, ToxIN, functions as a protein-RNA toxin-antitoxin pair

DOI: 10.1073/pnas.0808832106 DOI Help
PMID: 19124776 PMID Help

Authors: P. C. Fineran (University of Cambridge) , T. R. Blower (University of Cambridge) , I. J. Foulds (University of Cambridge) , D. P. Humphreys (UCB-Celltech) , K. S. Lilley (University of Cambridge) , G. P. C. Salmond (University of Cambridge)
Co-authored by industrial partner: No

Type: Journal Paper
Journal: Proceedings Of The National Academy Of Sciences , VOL 106 (3) , PAGES 894 - 899

State: Published (Approved)
Published: January 2009

Open Access Open Access

Abstract: Various mechanisms exist that enable bacteria to resist bacteriophage infection. Resistance strategies include the abortive infection (Abi) systems, which promote cell death and limit phage replication within a bacterial population. A highly effective 2-gene Abi system from the phytopathogen Erwinia carotovora subspecies atroseptica, designated ToxIN, is described. The ToxIN Abi system also functions as a toxin–antitoxin (TA) pair, with ToxN inhibiting bacterial growth and the tandemly repeated ToxI RNA antitoxin counteracting the toxicity. TA modules are currently divided into 2 classes, protein and RNA antisense. We provide evidence that ToxIN defines an entirely new TA class that functions via a novel protein-RNA mechanism, with analogous systems present in diverse bacteria. Despite the debated role of TA systems, we demonstrate that ToxIN provides viral resistance in a range of bacterial genera against multiple phages. This is the first demonstration of a novel mechanistic class of TA systems and of an Abi system functioning in different bacterial genera, both with implications for the dynamics of phage-bacterial interactions.

Journal Keywords: Bacterial; Bacteriophages; Base; Escherichia; Pectobacterium; Plasmids; RNA

Subject Areas: Biology and Bio-materials


Instruments: I03-Macromolecular Crystallography

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