Passive abortive infection mechanisms targeting phage long tail fiber proteins

Bacteria employ diverse defense strategies against phage infection, yet mechanisms directly targeting viral proteins remain scarcely documented. In this study, we characterize two bacterial defense systems: TFAD1 featuring a serine protease and TFAD2 featuring a Ser/Thr kinase. We show that TFAD1 and TFAD2 act on phage long tail fiber proteins via protein degradation and phosphorylation, respectively. Intriguingly, both systems allow complete phage replication cycles but generate non-infective progeny—a mechanism distinct from classical abortive infection (Abi), which we term “passive Abi”. Our findings expand the paradigm of bacterial immunity by unveiling protease- and kinase-mediated incapacitation of phage structural proteins, offering insights into the molecular arms race between bacteria and phages.