Phage single-stranded DNA-binding protein or host DNA damage triggers the activation of the AbpAB phage defense system

Bacteria have developed various defense mechanisms against phages. Abortive infection (Abi), a bacterial defense mechanism, can be achieved through various means, including toxin-antitoxin systems, cyclic oligonucleotide-based antiphage signaling systems, and retrons. AbpA and AbpB (AbpAB) defend against many lytic phages harboring double-stranded DNA genomes in Escherichia coli; however, how AbpAB senses phage infection and inhibits its propagation remains unclear. Here, we demonstrated that AbpAB inhibited the growth of the phi X174 lytic phage with single-stranded DNA (ssDNA) as well as the lysogenization and induction of the Sakai prophage 5 lysogenic phage. The AbpAB defense system limits T4 and phi X174 phage propagation via Abi. AbpA contains a nuclease domain at its N-terminus, and AbpB has an ATP-dependent RNA helicase domain; both domains are required for phage defense. This system is activated by phage Gp32 binding to ssDNA and inhibits E. coli growth. Without phage infection, DNA replication inhibitors or defects in the DNA repair factors RecB and RecC activate this system. Therefore, the E. coli AbpAB defense system may sense DNA-protein complexes, including the phage-encoded ssDNA-binding protein or those formed by interrupting host DNA replication or repair.