Quorum sensing is a process of chemical communication that bacteria use to track cell density and coordinate gene expression across a population. Bacteria-infecting viruses, called phages, can encode quorum-sensing components that enable them to integrate host cell density information into the lysis-lysogeny decision. Vibriophage VP882 is one such phage, and activation of its quorum-sensing pathway leads to the production of an antirepressor called Qtip. Qtip interferes with the prophage repressor (cIVP882), leading to host-cell lysis. Here, we show that Qtip interacts with the N terminus of cIVP882, inhibiting both cIVP882 DNA binding and cIVP882 autoproteolysis. Qtip also sequesters cIVP882, localizing it to the poles. Qtip can localize to the poles independently of cIVP882. Alanine-scanning mutagenesis of Qtip shows that its localization and interference with cIVP882 activities are separable. Comparison of Qtip to a canonical phage antirepressor reveals that despite both proteins interacting with their partner repressors, only Qtip drives polar localization.

中文翻译：

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噬菌体编码的群体感应激活的抗阻遏物 Qtip 的分离功能。

群体感应是一种化学通讯过程，细菌使用它来跟踪细胞密度和协调整个群体的基因表达。被称为噬菌体的细菌感染病毒可以编码群体感应成分，使它们能够将宿主细胞密度信息整合到裂解-溶原性决策中。Vibriophage VP882 就是这样一种噬菌体，激活其群体感应途径会导致产生一种称为 Qtip 的抗阻遏物。Qtip 干扰前噬菌体阻遏物 (cIVP882)，导致宿主细胞裂解。在这里，我们展示了 Qtip 与 cIVP882 的 N 末端相互作用，抑制 cIVP882 DNA 结合和 cIVP882 自身蛋白水解。Qtip 还隔离 cIVP882，将其定位到两极。Qtip 可以独立于 cIVP882 定位到极点。Qtip 的丙氨酸扫描诱变显示其定位和干扰 cIVP882 活动是可分离的。将 Qtip 与典型的噬菌体抗阻遏物进行比较表明，尽管两种蛋白质都与它们的伴侣阻遏物相互作用，但只有 Qtip 驱动极性定位。