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遗传修饰沙门氏菌膜物理状态改变了热休克反应的模式。

Genetic modification of the Salmonella membrane physical state alters the pattern of heat shock response.

机构信息

University of Salerno, Department of Pharmaceutical Sciences, Faculty of Pharmacy, Division of BioMedicine, Salerno, Italy.

出版信息

J Bacteriol. 2010 Apr;192(7):1988-98. doi: 10.1128/JB.00988-09. Epub 2010 Feb 5.

Abstract

It is now recognized that membranes are not simple physical barriers but represent a complex and dynamic environment that affects membrane protein structures and their functions. Recent data emphasize the role of membranes in sensing temperature changes, and it has been shown that the physical state of the plasma membrane influences the expression of a variety of genes such as heat shock genes. It has been widely shown that minor alterations in lipid membranes are critically involved in the conversion of signals from the environment to the transcriptional activation of heat shock genes. Previously, we have proposed that the composition, molecular arrangement, and physical state of lipid membranes and their organization have crucial roles in cellular responses during stress caused by physical and chemical factors as well as in pathological states. Here, we show that transformation of Salmonella enterica serovar Typhimurium LT2 (Salmonella Typhimurium) with a heterologous Delta(12)-desaturase (or with its trans-membrane regions) causes major changes in the pathogen's membrane dynamic. In addition, this pathogen is strongly impaired in the synthesis of major stress proteins (heat shock proteins) under heat shock. These data support the hypothesis that the perception of temperature in Salmonella is strictly controlled by membrane order and by a specific membrane lipid/protein ratio that ultimately causes transcriptional activation of heat shock genes. These results represent a previously unrecognized mode of sensing temperature variation used by this pathogen at the onset of infection.

摘要

现在人们已经认识到,膜并不是简单的物理屏障,而是代表了一个复杂而动态的环境,影响着膜蛋白的结构及其功能。最近的数据强调了膜在感知温度变化方面的作用,并且已经表明质膜的物理状态会影响多种基因的表达,如热休克基因。人们已经广泛证明,脂质膜的微小变化在将环境信号转化为热休克基因的转录激活方面起着至关重要的作用。以前,我们曾提出脂质膜的组成、分子排列和物理状态及其组织在细胞对物理和化学因素以及病理状态引起的应激的反应中起着关键作用。在这里,我们表明,用异源的 Delta(12)-去饱和酶(或其跨膜区域)转化沙门氏菌肠亚种 Typhimurium LT2(鼠伤寒沙门氏菌)会导致病原体膜动态的重大变化。此外,这种病原体在热休克下合成主要应激蛋白(热休克蛋白)的能力受到严重损害。这些数据支持了这样一种假设,即沙门氏菌对温度的感知受到膜有序性和特定膜脂/蛋白比的严格控制,最终导致热休克基因的转录激活。这些结果代表了这种病原体在感染开始时用于感知温度变化的一种以前未被认识的模式。

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