Re-evaluating the role of hok /Sok in T4 phage defense

The hok /Sok toxin-antitoxin system was shown to protect Escherichia coli BK6 from the T4 phage at low multiplicity of infection. One proposed mechanism relies on the rapid depletion of the Sok RNA antitoxin after T4-induced transcriptional arrest, allowing Hok toxin translation. In this model, Hok-mediated cell death prevents phage replication, acting as an altruistic defense system to limit infection spread. Here, we showed that the presence of hok /Sok is not sufficient to protect E. coli against phage T4 infection. Our findings point to a gap in our understanding of the requirements for phage defense mediated by hok /Sok.