Department of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Howard Hughes Medical Institute, Chevy Chase, Maryland, United States of America.
PLoS Genet. 2024 Jul 30;20(7):e1011243. doi: 10.1371/journal.pgen.1011243. eCollection 2024 Jul.
Quorum sensing (QS) is a process of cell-to-cell communication that bacteria use to synchronize collective behaviors. QS relies on the production, release, and group-wide detection of extracellular signaling molecules called autoinducers. Vibrios use two QS systems: the LuxO-OpaR circuit and the VqmA-VqmR circuit. Both QS circuits control group behaviors including biofilm formation and surface motility. The Vibrio parahaemolyticus temperate phage φVP882 encodes a VqmA homolog (called VqmAφ). When VqmAφ is produced by φVP882 lysogens, it binds to the host-produced autoinducer called DPO and launches the φVP882 lytic cascade. This activity times induction of lysis with high host cell density and presumably promotes maximal phage transmission to new cells. Here, we explore whether, in addition to induction from lysogeny, QS controls the initial establishment of lysogeny by φVP882 in naïve host cells. Using mutagenesis, phage infection assays, and phenotypic analyses, we show that φVP882 connects its initial lysis-lysogeny decision to both host cell density and whether the host resides in liquid or on a surface. Host cells in the low-cell-density QS state primarily undergo lysogenic conversion. The QS regulator LuxO~P promotes φVP882 lysogenic conversion of low-cell-density planktonic host cells. By contrast, the ScrABC surface-sensing system regulates lysogenic conversion of low-cell-density surface-associated host cells. ScrABC controls the abundance of the second messenger molecule cyclic diguanylate, which in turn, modulates motility. The scrABC operon is only expressed when its QS repressor, OpaR, is absent. Thus, at low cell density, QS-dependent derepression of scrABC drives lysogenic conversion in surface-associated host cells. These results demonstrate that φVP882 integrates cues from multiple sensory pathways into its lifestyle decision making upon infection of a new host cell.
群体感应（QS）是一种细菌之间的细胞通讯过程，用于协调集体行为。QS 依赖于胞外信号分子（称为自动诱导剂）的产生、释放和全群检测。弧菌使用两种 QS 系统：LuxO-OpaR 回路和 VqmA-VqmR 回路。这两个 QS 回路控制群体行为，包括生物膜形成和表面运动。副溶血弧菌温和噬菌体 φVP882 编码一个 VqmA 同源物（称为 VqmAφ）。当 VqmAφ 由 φVP882 溶原菌产生时，它与宿主产生的自动诱导剂 DPO 结合，并启动 φVP882 的裂解级联反应。这种活性与高宿主细胞密度下的裂解诱导相结合，推测可促进噬菌体最大程度地传递给新细胞。在这里，我们探讨了除了从溶原菌诱导之外，QS 是否还控制 φVP882 在宿主细胞中初始建立溶原菌。通过突变、噬菌体感染实验和表型分析，我们发现 φVP882 将其最初的裂解-溶原决定与宿主细胞密度以及宿主是否存在于液体中或表面上联系起来。低细胞密度 QS 状态下的宿主细胞主要经历溶原性转化。QS 调节因子 LuxO~P 促进 φVP882 对低细胞密度浮游宿主细胞的溶原性转化。相比之下，ScrABC 表面感应系统调节低细胞密度表面相关宿主细胞的溶原性转化。ScrABC 控制第二信使分子环二鸟苷酸的丰度，从而调节运动性。只有当 QS 抑制剂 OpaR 不存在时，scrABC 操纵子才会表达。因此，在低细胞密度下，QS 依赖性 scrABC 去阻遏驱动表面相关宿主细胞中的溶原性转化。这些结果表明，当感染新宿主细胞时，φVP882 将来自多个感应途径的线索整合到其生活方式决策中。
