Anti-viral defence by an mRNA ADP-ribosyltransferase that blocks translation.

ABSTRACT: Host-pathogen conflicts are crucibles of molecular innovation^1,2. Selection for immunity to pathogens has driven the evolution of sophisticated immunity mechanisms throughout biology, including in bacterial defence against bacteriophages³. Here we characterize the widely distributed anti-phage defence system CmdTAC, which provides robust defence against infection by the T-even family of phages⁴. Our results support a model in which CmdC detects infection by sensing viral capsid proteins, ultimately leading to the activation of a toxic ADP-ribosyltransferase effector protein, CmdT. We show that newly synthesized capsid protein triggers dissociation of the chaperone CmdC from the CmdTAC complex, leading to destabilization and degradation of the antitoxin CmdA

SUBMITTER: Vassallo CN 

PROVIDER: S-EPMC11618068 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature