Quorum sensing in Yersinia enterocolitica controls swimming and swarming motility
Quorum sensing in Yersinia enterocolitica controls swimming and swarming motility
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DOI：
10.1128/jb.188.4.1451-1461.2006
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发表时间：
2006-02-01
影响因子：
3.2
通讯作者：
Williams, P
中科院分区：
文献类型：
--
作者：
Atkinson, S;Chang, CY;Williams, P
小肠结肠耶尔森菌LuxI同源物YenI指导N-3-（氧己基）高丝氨酸内酯（3-氧己基C6-HSL）和n -己基高丝氨酸内酯（C6-HSL）的合成。在小肠结肠炎y突变体中，游泳运动暂时延迟，而群体运动被取消。由于游泳和群集都依赖于鞭毛，我们从亲本和yenI突变体中纯化了鞭毛蛋白。电泳显示，与亲本菌株相比，在26℃下生长17 h的yenI突变体缺乏45 kda的鞭毛蛋白FleB。逆转录pcr结果显示，yenI突变对yenR、flhDC（运动主调控因子）和fliA（鞭毛sigma因子）表达无影响，而鞭毛蛋白结构基因fleB表达下调。由于3-oxo-C6-HSL和C6-HSL在yenI突变体中没有恢复游泳或群集，我们重新检查了小肠结肠炎耶氏菌的n -酰基高丝氨酸内酯（AHL）图谱。利用AHL生物传感器和质谱技术，我们鉴定了通过YenI合成的另外三个AHL: N-（3-氧十二烷基）高丝氨酸内酯、N-（3-氧十二烷基）高丝氨酸内酯（3-氧- c12 - hsl）和N-（3-氧十四烷基）高丝氨酸内酯。然而，无论是单独使用长链ahl还是与短链ahl结合使用，都不能恢复yenI突变体的群集或游泳。通过研究放射性标记的3-oxo-C12-HSL的转运，并将AHL生物传感器引入到yenI突变体中，我们证明外源AHL无法恢复yenI突变体的运动性与缺乏AHL摄取无关。然而，通过将yenI突变体与质粒携带的yenI拷贝互补，AHL的合成和活力都得到了恢复。
The Yersinia enterocolitica LuxI homologue YenI directs the synthesis of N-3-(oxohexanoyl)homoserine lactone (3-oxo-C6-HSL) and N-hexanoylhomoserine lactone (C6-HSL). In a Y. enterocolitica yenI mutant, swimming motility is temporally delayed while swarming motility is abolished. Since both swimming and swarming are flagellum dependent, we purified the flagellin protein from the parent and yenI mutant. Electrophoresis revealed that in contrast to the parent strain, the yenI mutant grown for 17 h at 26 degrees C lacked the 45-kDa flagellin protein FleB. Reverse transcription-PCR indicated that while mutation of yenI had no effect on yenR,flhDC (the motility master regulator) or fliA (the flagellar sigma factor) expression,fleB (the flagellin structural gene) was down-regulated. Since 3-oxo-C6-HSL and C6-HSL did not restore swimming or swarming in the yenI mutant, we reexamined the N-acylhomoserine lactone (AHL) profile of Y. enterocolitica. Using AHL biosensors and mass spectrometry, we identified three additional AHLs synthesized via YenI: N-(3-oxodecanoyl)bomoserine lactone, N-(3-oxododecanoyl)homoserine lactone (3-oxo-C12-HSL), and N-(3-oxotetrade-canoyl)homoserine lactone. However, none of the long-chain AHLs either alone or in combination with the short-chain AHLs restored swarming or swimming in the yenI mutant. By investigating the transport of radiolabeled 3-oxo-C12-HSL and by introducing an AHL biosensor into the yenI mutant we demonstrate that the inability of exogenous AHLs to restore motility to the yenI mutant is not related to a lack of AHL uptake. However, both AHL synthesis and motility were restored by complementation of the yenI mutant with a plasmid-borne copy of yenI.