Shivaji S, Prakash Jogadhenu S S
Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad, 500 007, India.
Arch Microbiol. 2010 Feb;192(2):85-95. doi: 10.1007/s00203-009-0539-y. Epub 2010 Jan 5.
Rigidification of the membrane appears to be the primary signal perceived by a bacterium when exposed to low temperature. The perception and transduction of the signal then occurs through a two-component signal transduction pathway consisting of a membrane-associated sensor and a cytoplasmic response regulator and as a consequence a set of cold-regulated genes are activated. In addition, changes in DNA topology due to change in temperature may also trigger cold-responsive mechanisms. Inducible proteins thus accumulated repair the damage caused by cold stress. For example, the fluidity of the rigidified membrane is restored by altering the levels of saturated and unsaturated fatty acids, by altering the fatty acid chain length, by changing the proportion of cis to trans fatty acids and by changing the proportion of anteiso to iso fatty acids. Bacteria could also achieve membrane fluidity changes by altering the protein content of the membrane and by altering the levels of the type of carotenoids synthesized. Changes in RNA secondary structure, changes in translation and alteration in protein conformation could also act as temperature sensors. This review highlights the various strategies by which bacteria senses low temperature signal and as to how it responds to the change.
当暴露于低温环境时，细胞膜的僵化似乎是细菌感知到的主要信号。信号的感知和转导随后通过一个双组分信号转导途径发生，该途径由一个与膜相关的传感器和一个细胞质响应调节因子组成，结果是一组冷调节基因被激活。此外，由于温度变化导致的DNA拓扑结构变化也可能触发冷响应机制。如此积累的诱导蛋白修复冷应激造成的损伤。例如，通过改变饱和脂肪酸和不饱和脂肪酸的水平、改变脂肪酸链长度、改变顺式脂肪酸与反式脂肪酸的比例以及改变anteiso脂肪酸与iso脂肪酸的比例，僵化细胞膜的流动性得以恢复。细菌还可以通过改变膜的蛋白质含量以及改变合成的类胡萝卜素类型的水平来实现膜流动性的变化。RNA二级结构的变化、翻译的变化以及蛋白质构象的改变也可以充当温度传感器。这篇综述强调了细菌感知低温信号的各种策略以及它如何应对这种变化。
