Temperature sensing by membranes.

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.