Natural Silencing of Quorum-Sensing Activity Protects from Lysis by an Autoinducer-Detecting Phage.

Quorum sensing (QS) is a chemical communication process that bacteria use to track population density and orchestrate collective behaviors. QS relies on the production, accumulation, and group-wide detection of extracellular signal molecules called autoinducers. Vibriophage 882 (phage VP882), a bacterial virus, encodes a homolog of the QS receptor-transcription factor, called VqmA, that monitors the QS autoinducer DPO. Phage VqmA binds DPO at high host-cell density and activates transcription of the phage gene . Qtip, an antirepressor, launches the phage lysis program. Phage-encoded VqmA when bound to DPO also manipulates host QS by activating transcription of the host gene . VqmR is a small RNA that controls downstream QS target genes. Here, we sequence strain O3:K6 882, the strain from which phage VP882 was initially isolated. The chromosomal region normally encoding and harbors a deletion encompassing and a portion of the promoter, inactivating that QS system. We discover that strain O3:K6 882 is also defective in its other QS systems, due to a mutation in , encoding the central QS transcriptional regulator LuxO. Both the and mutations lock strain O3:K6 882 into the low-cell density QS state. Reparation of the QS defects in strain O3:K6 882 promotes activation of phage VP882 lytic gene expression and LuxO is primarily responsible for this effect. Phage VP882-infected QS-competent strain O3:K6 882 cells lyse more rapidly and produce more viral particles than the QS-deficient parent strain. We propose that, in strain O3:K6 882, constitutive maintenance of the low-cell density QS state suppresses the launch of the phage VP882 lytic cascade, thereby protecting the bacterial host from phage-mediated lysis.