Institute of Biochemistry, Biol. Res. Centre, Hungarian Acad. Sci., Temesvári krt. 62, H-6734 Szeged, Hungary.
Prog Lipid Res. 2012 Jul;51(3):208-20. doi: 10.1016/j.plipres.2012.02.002. Epub 2012 Mar 29.
The ability of photosynthetic organisms to adapt to increases in environmental temperatures is becoming more important with climate change. Heat stress is known to induce heat-shock proteins (HSPs) many of which act as chaperones. Traditionally, it has been thought that protein denaturation acts as a trigger for HSP induction. However, increasing evidence has shown that many stress events cause HSP induction without commensurate protein denaturation. This has led to the membrane sensor hypothesis where the membrane's physical and structural properties play an initiating role in the heat shock response. In this review, we discuss heat-induced modulation of the membrane's physical state and changes to these properties which can be brought about by interaction with HSPs. Heat stress also leads to changes in lipid-based signaling cascades and alterations in calcium transport and availability. Such observations emphasize the importance of membranes and their lipids in the heat shock response and provide a new perspective for guiding further studies into the mechanisms that mediate cellular and organismal responses to heat stress.
随着气候变化,光合生物适应环境温度升高的能力变得越来越重要。众所周知,热应激会诱导热休克蛋白(HSPs),其中许多 HSP 作为分子伴侣发挥作用。传统上,人们认为蛋白质变性是 HSP 诱导的触发因素。然而,越来越多的证据表明,许多应激事件会导致 HSP 诱导,而蛋白质没有相应的变性。这导致了膜传感器假说,其中膜的物理和结构特性在热休克反应中发挥启动作用。在这篇综述中,我们讨论了热诱导的膜物理状态的调制以及与 HSPs 相互作用可以带来的这些性质的变化。热应激还会导致基于脂质的信号级联的变化以及钙运输和可用性的改变。这些观察结果强调了膜及其脂质在热休克反应中的重要性,并为进一步研究介导细胞和生物体对热应激反应的机制提供了新的视角。