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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Autoinducer-mediated regulation of rhamnolipid biosurfactant synthesis in Pseudomonas aeruginosa.
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Autoinducer-mediated regulation of rhamnolipid biosurfactant synthesis in Pseudomonas aeruginosa.

机译：自动诱导物介导的铜绿假单胞菌鼠李糖脂生物表面活性剂合成的调控。

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摘要

The opportunistic human pathogen Pseudomonas aeruginosa produces a variety of virulence factors, including exotoxin A, elastase, alkaline protease, alginate, phospholipases, and extracellular rhamnolipids. The previously characterized rhlABR gene cluster encodes a regulatory protein (RhlR) and a rhamnosyltransferase (RhlAB), both of which are required for rhamnolipid synthesis. Another gene, rhII, has now been identified downstream of the rhlABR gene cluster. The putative RhlI protein shares significant sequence similarity with bacterial autoinducer synthetases of the LuxI type. A P. aeruginosa rhlI mutant strain carrying a disrupted rhlI gene was unable to produce rhamnolipids and lacked rhamnosyltransferase activity. Rhamnolipid synthesis was restored by introducing a wild-type rhlI gene into such strains or, alternatively, by adding either the cell-free spent supernatant from a P. aeruginosa wild-type strain or synthetic N-acylhomoserine lactones. Half-maximal induction of rhamnolipid synthesis in the rhlI mutant strain required 0.5 microM N-butyrylhomoserine lactone or 10 microM N-(3-oxohexanoyl)homoserine lactone. The P. aeruginosa rhlA promoter was active in the heterologous host Pseudomonas putida when both the rhlR and rhlI genes were present or when the rhlR gene alone was supplied together with synthetic N-acylhomoserine lactones. The RhlR-RhlI regulatory system was found to be essential for the production of elastase as well, and cross-communication between the RhlR-RhlI rhamnolipid regulatory system and the LasR-LasI elastase regulatory system was demonstrated.
机译：机会性人类病原体铜绿假单胞菌产生多种毒力因子，包括外毒素A，弹性蛋白酶，碱性蛋白酶，藻酸盐，磷脂酶和胞外鼠李糖脂。先前表征的rhlABR基因簇编码调控蛋白（RhlR）和鼠李糖基转移酶（RhlAB），这两者都是鼠李糖脂合成所必需的。现已在rhlABR基因簇的下游发现了另一个基因rhII。推定的RhlI蛋白与LuxI型细菌自诱导合成具有明显的序列相似性。携带破坏的rhlI基因的铜绿假单胞菌rhlI突变株不能产生鼠李糖脂并且缺乏鼠李糖基转移酶活性。通过将野生型rhlI基因导入此类菌株中，或通过添加来自铜绿假单胞菌野生型菌株的无细胞废上清液或合成的N-酰基高丝氨酸内酯，恢复鼠李糖脂的合成。 rhlI突变菌株中鼠李糖脂合成的半数最大诱导需要0.5 microM N-丁酰高丝氨酸内酯或10 microM N-（3-氧代己酰）高丝氨酸内酯。当rhR和rhI基因同时存在或单独提供rhR基因和合成的N-酰基高丝氨酸内酯时，铜绿假单胞菌rhA启动子在异源恶臭假单胞菌中有活性。还发现，RhlR-RhlI调节系统对于生产弹性蛋白酶也是必不可少的，并且证明了RhlR-RhlI鼠李糖脂调节系统和LasR-LasI弹性蛋白酶调节系统之间的交叉通讯。

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