A phage-encoded RNA-binding protein inhibits the antiviral activity of a toxin-antitoxin system.
Ontology highlight
ABSTRACT: Bacteria harbor diverse mechanisms to defend themselves against their viral predators, bacteriophages. In response, phages can evolve counter-defense systems, most of which are poorly understood. In T4-like phages, the gene tifA prevents bacterial defense by the type III toxin-antitoxin (TA) system toxIN, but the mechanism by which TifA inhibits ToxIN remains unclear. Here, we show that TifA directly binds both the endoribonuclease ToxN and RNA, leading to the formation of a high molecular weight ribonucleoprotein complex in which ToxN is inhibited. The RNA binding activity of TifA is necessary for its interaction with and inhibition of ToxN. Thus, we propose that TifA inhibits ToxN during phage infection by trapping ToxN on cellular RNA, particularly the abundant 16S rRNA, thereby prevent
SUBMITTER: Guegler CK
PROVIDER: S-EPMC10853763 | biostudies-literature | 2024 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA