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A processed non-coding RNA regulates a bacterial antiviral systemA processed non-coding RNA regulates a bacterial antiviral system
Structural highlights
FunctionTOXN_PECAT Toxic component of a type III toxin-antitoxin (TA) system. An endoribonuclease which is active independently of the ribosome, cleaving between the second and third A of AAA(U/G) sequences, although not all occurrences of this tetranucleotide are cleaved (PubMed:23267117). Digests many mRNA species, including its own transcript and its cognate antitoxin RNA ToxI. ToxI has 5.5 nearly identical 36 nucleotide-long repeats (a single repeat neutralizes the toxin in vivo); a single repeat folds into a pseudoknot which binds the toxin (PubMed:21240270). The ToxI precursor RNA is a preferential target in vivo and is progressively degraded to single repeat lengths as ToxN-ToxI complex self-assembly occurs (PubMed:23267117). In vivo expression of ToxI antitoxin inhibits endonuclease activity of ToxN (PubMed:23267117). The toxin alone inhibits growth when expressed in E.coli without causing cell lysis; this bacteriostatic effect is neutralized by cognate RNA antitoxin ToxI (PubMed:19124776, PubMed:23267117). Non-cognate antitoxin RNA from B.thuringiensis does not inhibit this toxin (PubMed:23267117). The RNA antitoxin is less stable than the proteinaceous toxin; synthesis of ToxI in the absence of new ToxN synthesis restores growth and also detectable accumulation of the ToxN protein (PubMed:19124776). Negatively regulates its own operon in complex with ToxI (PubMed:19633081). The toxin-antitoxin system functions in plasmid maintenance (a plasmid addiction system) (PubMed:23267117).[1] [2] [3] [4] The TA system protects P.atrosepticum strain 1043 against phage phiM1 and phiA2, E.coli against some but not all coliphages and S.marcescens against some bacteriophages, causing an abortive infection (Abi phenotype) (PubMed:19124776). Also protects P.atrosepticum strain 1043 against phage phiTE; phage that escape Abi and grow in this bacterium have evolved a pseudo-ToxI RNA by expanding a pre-existing sequence similar to the bona fide ToxI repeats (PubMed:23109916).[5] [6] Publication Abstract from PubMedVarious 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. The phage abortive infection system, ToxIN, functions as a protein-RNA toxin-antitoxin pair.,Fineran PC, Blower TR, Foulds IJ, Humphreys DP, Lilley KS, Salmond GP Proc Natl Acad Sci U S A. 2009 Jan 20;106(3):894-9. Epub 2009 Jan 5. PMID:19124776[7] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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