Acyl-homoserine lactone (AHL) is the most studied autoinducer in gram-negative bacteria controlling infections of various pathogens. Quenching of AHL signaling by inhibiting AHL synthesis or AHL-receptor binding via small molecular chemicals or enzymatically degrading AHL is commonly used to block bacterial infections. Here, we describe a new quorum-quenching strategy that directly “acquires” bacterial genes/proteins through a defined platform. We artificially expressed a typical AHL synthase gene from the biocontrol 2P24 in the antifungal bacterium OH11 lacking AHL production. This step led to the discovery of multiple PcoI interacting protein candidates from . The individual expression of these candidate genes in 2P24 led to the identification of Le0959, which encodes leucyl aminopeptidase, an effective protein that inhibits AHL synthesis in 2P24. Therefore, we define Le0959 as LqqP (uorum-uenching rotein). The expression of in could produce AHL, and the introduction of into expressing could prevent the production of AHL. LqqP directly binds to PcoI, and this protein–protein binding reduced the abundance of free PcoI (capable of AHL synthesis) , thereby blocking PcoI-dependent AHL production. Overall, this study highlights the discovery of LqqP in quenching AHL quorum sensing by binding to AHL synthase via developing a previously-uncharacterized screening technique for bacterial quorum quenching.

中文翻译：

---

溶杆菌亮氨肽酶的细菌群体感应猝灭活性通过与自诱导剂合酶相互作用起作用


酰基高丝氨酸内酯 (AHL) 是控制各种病原体感染的革兰氏阴性菌中研究最多的自诱导剂。通过小分子化学物质抑制 AHL 合成或 AHL 受体结合或酶促降解 AHL 来猝灭 AHL 信号传导，通常用于阻止细菌感染。在这里，我们描述了一种新的群体淬灭策略，通过定义的平台直接“获取”细菌基因/蛋白质。我们在缺乏 AHL 产生的抗真菌细菌 OH11 中人工表达了来自生物对照 2P24 的典型 AHL 合酶基因。这一步骤导致从 中发现了多个 PcoI 相互作用蛋白候选物。这些候选基因在 2P24 中的单独表达导致了 Le0959 的鉴定，它编码亮氨酰氨肽酶，这是一种抑制 2P24 中 AHL 合成的有效蛋白质。因此，我们将Le0959定义为LqqP（uorum-uenching rotein）。 in的表达可以产生AHL，引入in的表达可以阻止AHL的产生。 LqqP 直接与 PcoI 结合，这种蛋白质-蛋白质结合减少了游离 PcoI（能够合成 AHL）的丰度，从而阻断了 PcoI 依赖性 AHL 的产生。总体而言，本研究强调了通过开发一种先前未表征的细菌群体淬灭筛选技术，LqqP 通过与 AHL 合酶结合来淬灭 AHL 群体感应的发现。