Poolman Bert, Blount Paul, Folgering Joost H A, Friesen Robert H E, Moe Paul C, van der Heide Tiemen
Department of Biochemistry, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Nijenborgh, Groningen, The Netherlands.
Mol Microbiol. 2002 May;44(4):889-902. doi: 10.1046/j.1365-2958.2002.02894.x.
Maintenance of cell turgor is a prerequisite for almost any form of life as it provides a mechanical force for the expansion of the cell envelope. As changes in extracellular osmolality will have similar physicochemical effects on cells from all biological kingdoms, the responses to osmotic stress may be alike in all organisms. The primary response of bacteria to osmotic upshifts involves the activation of transporters, to effect the rapid accumulation of osmoprotectants, and sensor kinases, to increase the transport and/or biosynthetic capacity for these solutes. Upon osmotic downshift, the excess of cytoplasmic solutes is released via mechanosensitive channel proteins. A number of breakthroughs in the last one or two years have led to tremendous advances in our understanding of the molecular mechanisms of osmosensing in bacteria. The possible mechanisms of osmosensing, and the actual evidence for a particular mechanism, are presented for well studied, osmoregulated transport systems, sensor kinases and mechanosensitive channel proteins. The emerging picture is that intracellular ionic solutes (or ionic strength) serve as a signal for the activation of the upshift-activated transporters and sensor kinases. For at least one system, there is strong evidence that the signal is transduced to the protein complex via alterations in the protein-lipid interactions rather than direct sensing of ion concentration or ionic strength by the proteins. The osmotic downshift-activated mechanosensitive channels, on the other hand, sense tension in the membrane but other factors such as hydration state of the protein may affect the equilibrium between open and closed states of the proteins.
维持细胞膨压是几乎任何生命形式的先决条件，因为它为细胞膜的扩张提供了机械力。由于细胞外渗透压的变化会对所有生物界的细胞产生相似的物理化学作用，因此所有生物体对渗透胁迫的反应可能是相似的。细菌对渗透压升高的主要反应包括激活转运蛋白以实现渗透保护剂的快速积累，以及激活传感激酶以提高这些溶质的转运和/或生物合成能力。在渗透压降低时，过量的细胞质溶质通过机械敏感通道蛋白释放。过去一两年的一些突破使我们对细菌渗透压感知分子机制的理解取得了巨大进展。本文针对研究充分的渗透调节转运系统、传感激酶和机械敏感通道蛋白，介绍了可能的渗透压感知机制以及特定机制的实际证据。新出现的情况是，细胞内离子溶质（或离子强度）作为激活渗透压升高激活的转运蛋白和传感激酶的信号。至少对于一个系统，有强有力的证据表明，信号是通过蛋白质-脂质相互作用的改变而非蛋白质直接感知离子浓度或离子强度传递到蛋白质复合物的。另一方面，渗透压降低激活的机械敏感通道感知膜中的张力，但其他因素如蛋白质的水合状态可能会影响蛋白质开放和关闭状态之间的平衡。
