Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET) and Departamento de Microbiología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, 2000-Rosario, Argentina; email:
Annu Rev Microbiol. 2014;68:101-16. doi: 10.1146/annurev-micro-091313-103612. Epub 2014 May 7.
Bacteria remodel the fluidity of their membrane bilayer precisely via the incorporation of proportionally more unsaturated fatty acids (or fatty acids with analogous properties) as growth temperature decreases. This process, termed homoviscous adaptation, is suited to disrupt the order of the lipid bilayer and optimizes the performance of a large array of cellular physiological processes at the new temperature. As such, microbes have developed molecular strategies to sense changes in membrane fluidity, provoked by a decrease in environmental temperature, and initiate cellular responses that upregulate the biosynthesis of unsaturated fatty acids. This review focuses on the architecture of a membrane fluidity communication network; how thermal information is integrated, processed, and transduced to control gene expression; how membrane-mediated structural changes of a cold sensor are accomplished; and the intriguing possibility that temperature-induced deformations of the cell membrane act as allosteric regulators of protein function.
细菌通过在膜双层中掺入比例更高的不饱和脂肪酸（或具有类似特性的脂肪酸）来精确重塑膜双层的流动性，这种现象随着生长温度的降低而发生。这个过程被称为同型粘性适应，它能够破坏脂质双层的有序性，并优化大量细胞生理过程在新温度下的性能。因此，微生物已经发展出分子策略来感知由环境温度降低引起的膜流动性变化，并启动细胞响应，上调不饱和脂肪酸的生物合成。这篇综述重点介绍了膜流动性通讯网络的结构；热信息如何被整合、处理和转导以控制基因表达；冷感受器的膜介导结构变化是如何实现的；以及有趣的可能性，即细胞膜的温度诱导变形作为蛋白质功能的变构调节剂。
