Abstract: Bacteria are under constant attack from predatory bacteriophages in a co-evolutionary molecular “arms race”. Various mechanisms have evolved in bacteria in their adaptation to viral attack, including surface receptor mutation, restriction and modification, CRISPR-Cas systems and abortive infection (Abi). We have investigated a particular Abi system in the enterobacterial phytopathogen,Erwinia (Pectobacterium). This Abi system is encoded by a cryptic plasmid and is bi-functional in that it also has toxin-antitoxin (TA) traits. This Abi/TA mechanism defines the Type III class of TA systems in which a toxic endoribonuclease protein (ToxN) is suppressed by a small RNA (ToxI) encoded by repeat elements lying immediately upstream of the toxin gene. The Abi phenotype arises as a post-infection event thought to be through destabilisation of the ToxIN complex and release of the endoribonuclease which then degrades multiple target RNAs. The cognate genes for ToxI and ToxN are widely distributed in bacteria. Although the mature ToxIN (RNA-protein) complex efficiently aborts productive infection in various phages, some can evolve to “escape” the ToxIN system, through different mechanisms. One possible interpretation of the mode of action of this Type III TA/Abi system is that it may act as an “altruistic suicide” defence that allows bacterial populations to control the replication of their viral parasites.
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