In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 19, No. 7 ( 2023-7-31), p. e1010809-
Abstract:
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 Vibrio QS receptor-transcription factor, called VqmA, that monitors the Vibrio QS autoinducer DPO. Phage VqmA binds DPO at high host-cell density and activates transcription of the phage gene qtip . 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 . VqmR is a small RNA that controls downstream QS target genes. Here, we sequence Vibrio parahaemolyticus strain O3:K6 882, the strain from which phage VP882 was initially isolated. The chromosomal region normally encoding vqmR and vqmA harbors a deletion encompassing vqmR and a portion of the vqmA promoter, inactivating that QS system. We discover that V . parahaemolyticus strain O3:K6 882 is also defective in its other QS systems, due to a mutation in luxO , encoding the central QS transcriptional regulator LuxO. Both the vqmR-vqmA and luxO mutations lock V . parahaemolyticus strain O3:K6 882 into the low-cell density QS state. Reparation of the QS defects in V . parahaemolyticus 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 V . parahaemolyticus strain O3:K6 882 cells lyse more rapidly and produce more viral particles than the QS-deficient parent strain. We propose that, in V . parahaemolyticus 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.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010809
DOI:
10.1371/journal.pgen.1010809.g001
DOI:
10.1371/journal.pgen.1010809.g002
DOI:
10.1371/journal.pgen.1010809.g003
DOI:
10.1371/journal.pgen.1010809.g004
DOI:
10.1371/journal.pgen.1010809.g005
DOI:
10.1371/journal.pgen.1010809.g006
DOI:
10.1371/journal.pgen.1010809.s001
DOI:
10.1371/journal.pgen.1010809.s002
DOI:
10.1371/journal.pgen.1010809.s003
DOI:
10.1371/journal.pgen.1010809.s004
DOI:
10.1371/journal.pgen.1010809.s005
DOI:
10.1371/journal.pgen.1010809.s006
DOI:
10.1371/journal.pgen.1010809.s007
DOI:
10.1371/journal.pgen.1010809.s008
DOI:
10.1371/journal.pgen.1010809.s009
DOI:
10.1371/journal.pgen.1010809.s010
DOI:
10.1371/journal.pgen.1010809.s011
DOI:
10.1371/journal.pgen.1010809.s012
DOI:
10.1371/journal.pgen.1010809.r001
DOI:
10.1371/journal.pgen.1010809.r002
DOI:
10.1371/journal.pgen.1010809.r003
DOI:
10.1371/journal.pgen.1010809.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2186725-2
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