The phage abortive infection system, ToxIN, functions as a protein-RNA toxin-antitoxin pair.
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.
Fineran
Peter C
PC
Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.
Blower
Tim R
TR
Foulds
Ian J
IJ
Humphreys
David P
DP
Lilley
Kathryn S
KS
Salmond
George P C
GP
D000992:Antitoxins / Q000235:genetics*; D001427:Bacterial Toxins / Q000235:genetics*; D001435:Bacteriophages / Q000187:drug effects*; D001483:Base Sequence; D004926:Escherichia coli / Q000254:growth & development; D008969:Molecular Sequence Data; D016973:Pectobacterium carotovorum / Q000235:genetics* / Q000821:virology*; D010957:Plasmids; D012313:RNA / Q000235:genetics*
D000992:Antitoxins; D001427:Bacterial Toxins; D012313:RNA