Functional interplay between the Yersinia pseudotuberculosis YpsRI and YtbRI quorum sensing systems modulates swimming motility by controlling expression of flhDC and fliA
Functional interplay between the Yersinia pseudotuberculosis YpsRI and YtbRI quorum sensing systems modulates swimming motility by controlling expression of flhDC and fliA
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假结核耶尔森菌 YpsRI 和 YtbRI 群体感应系统之间的功能相互作用通过控制 flhDC 和 fliA 的表达来调节游泳运动
DOI：
10.1111/j.1365-2958.2008.06268.x
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发表时间：
2008-07-01
影响因子：
3.6
通讯作者：
Williams, Paul
中科院分区：
文献类型：
--
作者：
Atkinson, Steve;Chang, Chien-Yi;Williams, Paul
假结核耶尔森菌中的群体感应 (QS) 涉及两对 LuxRI 直向同源物（YpsRI 和 YtbRI）和多个 N-酰基高丝氨酸内酯 (AHL)。在 ypsI/ytbI 突变体中，AHL 合成被废除，在 ypsR/ytbR 双突变体中不受影响，在 ypsI/ytbR 突变体中大幅减少，表明 YpsR 和 YtbR 对于 AHL 合成都不是必需的。为了确定 YpsRI 和 YtbRI 之间的相互关系，我们构建了与 ypsR、ypsI、ytbR 和 ytbI 的染色体 lux-启动子融合体，并检查了它们在每个 QS 突变体背景中的表达。 YpsRI 系统负向自动调节自身，但正向调节 ytbRI 系统的表达，而 ytbRI 系统正向自动调节，但仅在 ytbI 表达水平上。 YtbRI 不控制 ypsR 或 ypsI 的表达。这种分层 QS 系统通过调节 flhDC 和 fliA 来控制游泳运动。通过 YtbI 合成的 AHL 发挥双重作用，与 YpsR 结合激活 flhDC，但与 YtbR 和 YpsR 结合抑制 fliA。在液体和平板测定中，在 ypsR 和 ypsI 突变体中观察到的早期运动开始在 ytbI、ytbR ypsI/ytbI、ypsR/ytbR 突变体中被消除，表明 QS 正向（通过 YtbRI）和负向（通过 YpsRI）调节运动。
Quorum sensing (QS) in Yersinia pseudotuberculosis involves two pairs of LuxRI orthologues (YpsRI and YtbRI) and multiple N-acylhomoserine lactones (AHLs). In a ypsI/ytbI mutant, AHL synthesis was abolished, unaffected in a ypsR/ytbR double mutant and substantially reduced in a ypsI/ytbR mutant, indicating that neither YpsR nor YtbR is essential for AHL synthesis. To determine the interrelationship between YpsRI and YtbRI we constructed chromosomal lux-promoter fusions to ypsR, ypsI, ytbR and ytbI and examined their expression in each of the QS mutant backgrounds. The YpsRI system negatively autoregulates itself but positively regulates the expression of the ytbRI system whereas the ytbRI system is positively autoregulated but only at the level of ytbI expression. YtbRI does not control expression of ypsR or ypsI. This hierarchical QS system controls swimming motility via regulation of flhDC and fliA. The AHLs synthesized via YtbI play a dual role, activating flhDC, in conjunction with YpsR but repressing fliA in conjunction with YtbR and YpsR. In liquid and plate assays, the early onset of motility observed in ypsR and ypsI mutants was abolished in ytbI, ytbR ypsI/ytbI, ypsR/ytbR mutants, indicating that QS regulates motility both positively (via YtbRI) and negatively (via YpsRI).