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渗透胁迫和磷酸盐限制会改变铜绿假单胞菌细胞间信号分子和鼠李糖脂生物表面活性剂的产生。

Osmotic stress and phosphate limitation alter production of cell-to-cell signal molecules and rhamnolipid biosurfactant by Pseudomonas aeruginosa.

作者信息

Bazire Alexis, Dheilly Alexandra, Diab Farès, Morin Danièle, Jebbar Mohamed, Haras Dominique, Dufour Alain

机构信息

Laboratoire de Biotechnologie et Chimie Marines, EA 3884, Université de Bretagne Sud, BP 92116, 56321 Lorient, France.

出版信息

FEMS Microbiol Lett. 2005 Dec 1;253(1):125-31. doi: 10.1016/j.femsle.2005.09.029. Epub 2005 Oct 5.

Abstract

In Pseudomonas aeruginosa, rhamnolipid production is controlled by the quorum-sensing system RhlRI, which itself depends on LasRI. These systems use cell-to-cell signal molecules: N-butyryl-l-homoserine lactone (C4-HSL) and N-(3-oxododecanoyl)-l-homoserine lactone (3OC(12)-HSL), respectively. Whereas both HSLs were produced in M63 medium, rhamnolipid synthesis was not achieved. Phosphate limitation reduced the HSL concentrations, while allowing rhamnolipid production. Hyperosmotic shock applied during the exponential growth phase stopped the accumulation of 3OC(12)-HSL, and prevented C4-HSL and rhamnolipid production. These defects result from lower expression of genes involved in C4-HSL and rhamnolipid syntheses. The osmoprotectant glycine betaine partially restored C4-HSL and rhamnolipid production.

摘要

在铜绿假单胞菌中,鼠李糖脂的产生受群体感应系统RhlRI控制,而RhlRI本身又依赖于LasRI。这些系统分别使用细胞间信号分子:N-丁酰基-L-高丝氨酸内酯(C4-HSL)和N-(3-氧代十二烷酰基)-L-高丝氨酸内酯(3OC(12)-HSL)。虽然两种HSL在M63培养基中均有产生,但未实现鼠李糖脂的合成。磷酸盐限制降低了HSL浓度,同时允许鼠李糖脂的产生。在指数生长期施加高渗休克会阻止3OC(12)-HSL的积累,并阻止C4-HSL和鼠李糖脂的产生。这些缺陷是由于参与C4-HSL和鼠李糖脂合成的基因表达降低所致。渗透保护剂甘氨酸甜菜碱部分恢复了C4-HSL和鼠李糖脂的产生。

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