Abstract

Vibriophage VP882 launches its lytic cascade upon detection of a quorum-sensing autoinducer produced by its bacterial host. This capability enables the phage to maximize transmission by transitioning from lysogeny to lysis only at high host cell density, when abundant host cells are present to infect. Here, we show that two different pathways can be triggered upon prophage induction. When the prophage is induced via quorum sensing, Qtip, an anti-repressor, inhibits the cI lysogeny maintenance protein, driving expression of the lysis genes. The phage can also launch a cascade that causes host growth arrest. In this case, cI derepresses two genes, one encoding a DksA homolog, TraRVP882, and one encoding a protein that we name QisA. TraRVP882 and QisA form a complex that causes host growth arrest, relying on RNAP-binding by TraRVP882. Phage VP882 quorum sensing also activates production of a protein we call QtiQ, which inactivates the QisA-TraRVP882 complex, reestablishing host cell growth. Thus, in the presence of QtiQ, the phage lysis program is enacted. To our knowledge, QtiQ is the first protein inactivator of a TraR or DksA-like homolog. By inducing growth arrest, phage VP882 may enable its host to survive under stress-inducing conditions, or the phage may delay host lysis until optimal conditions are met. In both cases, the phage thereby enhances its own prospects for spread.