Baysse Christine, Cullinane Méabh, Dénervaud Valérie, Burrowes Elizabeth, Dow J Maxwell, Morrissey John P, Tam Ling, Trevors Jack T, O'Gara Fergal
BIOMERIT Research Centre, Microbiology Department, University College Cork, National University of Ireland, Cork, Ireland.
Department of Environmental Biology, Rm 3220 Bovey Building, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
Microbiology (Reading). 2005 Aug;151(Pt 8):2529-2542. doi: 10.1099/mic.0.28185-0.
Changes in the cellular envelope are major physiological adaptations that occur when micro-organisms encounter extreme environmental conditions. An appropriate degree of membrane fluidity is crucial for survival, and alteration of membrane lipids is an essential adaptive response. Emerging data suggest that microbial cells may recognize alterations in their membrane viscosity resulting from certain environmental changes as a trigger for adaptive cellular responses. In Pseudomonas aeruginosa, the quorum-sensing (QS) system involves a complex regulatory circuitry that coordinates the expression of genes according to a critical population density. Interestingly, it has been shown that the QS system of P. aeruginosa can also be activated by nutritional stress, independently of the cell density, and therefore may be part of a more general adaptive response to stressful environmental conditions. In order to examine the proposed link between membrane properties and stress signalling, the effects of genetically engineered alterations of the membrane phospholipid composition of P. aeruginosa PAO1 on the activation of the stringent response and the QS system were examined. The lptA gene encoding a functional homologue of PlsC, an Escherichia coli enzyme that catalyses the second step of the phospholipid biosynthesis pathway, was identified and disrupted. Inactivation of lptA altered the fatty acid profile of phospholipids and the membrane properties, resulting in decreased membrane fluidity. This resulted in a premature production of the QS signals N-butanoyl- and N-hexanoyl-homoserine lactone (C4-HSL and C6-HSL) and a repression of 2-heptyl-3-hydroxy-4-quinolone (PQS) synthesis at later growth phases. The effects on C4- and C6-HSL depended upon the expression of relA, encoding the (p)ppGpp alarmone synthase, which was increased in the lptA mutant. Together, the findings support the concept that alterations in membrane properties can act as a trigger for stress-related gene expression.
细胞包膜的变化是微生物在遇到极端环境条件时发生的主要生理适应。适当程度的膜流动性对生存至关重要，而膜脂的改变是一种重要的适应性反应。新出现的数据表明，微生物细胞可能将某些环境变化导致的膜粘度改变识别为适应性细胞反应的触发因素。在铜绿假单胞菌中，群体感应（QS）系统涉及一个复杂的调控电路，该电路根据临界群体密度协调基因表达。有趣的是，已表明铜绿假单胞菌的QS系统也可由营养应激激活，与细胞密度无关，因此可能是对压力环境条件更普遍适应性反应的一部分。为了研究膜特性与应激信号之间的假定联系，研究了铜绿假单胞菌PAO1膜磷脂组成的基因工程改变对严紧反应和QS系统激活的影响。鉴定并破坏了编码PlsC功能同源物的lptA基因，PlsC是一种大肠杆菌酶，催化磷脂生物合成途径的第二步。lptA的失活改变了磷脂的脂肪酸谱和膜特性，导致膜流动性降低。这导致在生长后期过早产生QS信号N-丁酰基-和N-己酰基-高丝氨酸内酯（C4-HSL和C6-HSL），并抑制2-庚基-3-羟基-4-喹诺酮（PQS）的合成。对C4-和C6-HSL的影响取决于relA的表达，relA编码（p）ppGpp警报素合酶，其在lptA突变体中增加。总之，这些发现支持了膜特性改变可作为应激相关基因表达触发因素的概念。
