Abstract

Bacteria are susceptible to infection by their viral predators (bacteriophages; phages) – the most abundant biological entities on Earth. Bacteria have evolved diverse strategies for evading the lethal impacts of phage infection and, correspondingly, phages evolve to circumvent bacterial defensive systems – an eternal co-evolutionary “molecular arms race”. Abortive infection (Abi) systems in bacteria are post-infection defence mechanisms that terminate viral morphogenesis through a “suicide” of infected cells. In this way, phage replication is blocked precociously and sibling bacteria are not infected. Certain Abi systems have Type III toxin-antitoxin (TA) functionality where an endoribonuclease (toxin) is suppressed by small RNA species (antitoxin). After infection by phages the bifunctional Abi/TA system may release the toxin, killing the infected cell. Phages can evolve mutants that “escape” the Type III TA system by various routes, to enable a productive viral lytic cycle.