Tatsumi H, Furuichi T, Nakano M, Toyota M, Hayakawa K, Sokabe M, Iida H
Nagoya University Graduate School of Medicine, Nagoya, Japan.
Plant Biol (Stuttg). 2014 Jan;16 Suppl 1:18-22. doi: 10.1111/plb.12095. Epub 2013 Sep 9.
Mechanosensitive (MS) channels are expressed in a variety of cells. The molecular and biophysical mechanism involved in the regulation of MS channel activities is a central interest in basic biology. MS channels are thought to play crucial roles in gravity sensing in plant cells. To date, two mechanisms have been proposed for MS channel activation. One is that tension development in the lipid bilayer directly activates MS channels. The second mechanism proposes that the cytoskeleton is involved in the channel activation, because MS channel activities are modulated by pharmacological treatments that affect the cytoskeleton. We tested whether tension in the cytoskeleton activates MS channels. Mammalian endothelial cells were microinjected with phalloidin-conjugated beads, which bound to stress fibres, and a traction force to the actin cytoskeleton was applied by dragging the beads with optical tweezers. MS channels were activated when the force was applied, demonstrating that a sub-pN force to the actin filaments activates a single MS channel. Plants may use a similar molecular mechanism in gravity sensing, since the cytoplasmic Ca(2+) concentration increase induced by changes in the gravity vector was attenuated by potential MS channel inhibitors, and by actin-disrupting drugs. These results support the idea that the tension increase in actin filaments by gravity-dependent sedimentation of amyloplasts activates MS Ca(2+) -permeable channels, which can be the molecular mechanism of a Ca(2+) concentration increase through gravistimulation. We review recent progress in the study of tension sensing by actin filaments and MS channels using advanced biophysical methods, and discuss their possible roles in gravisensing.
机械敏感(MS)通道在多种细胞中表达。MS通道活性调节所涉及的分子和生物物理机制是基础生物学的核心研究内容。MS通道被认为在植物细胞的重力感知中起关键作用。迄今为止,已提出两种MS通道激活机制。一种是脂质双分子层中的张力发展直接激活MS通道。第二种机制认为细胞骨架参与通道激活,因为MS通道活性受到影响细胞骨架的药物处理的调节。我们测试了细胞骨架中的张力是否激活MS通道。将与鬼笔环肽偶联的珠子显微注射到哺乳动物内皮细胞中,这些珠子与应力纤维结合,然后用光学镊子拖动珠子,对肌动蛋白细胞骨架施加牵引力。施加力时MS通道被激活,表明对肌动蛋白丝施加亚皮牛顿力可激活单个MS通道。植物在重力感知中可能使用类似的分子机制,因为重力矢量变化引起的细胞质Ca(2+)浓度增加会被潜在的MS通道抑制剂和破坏肌动蛋白的药物减弱。这些结果支持这样一种观点,即淀粉体的重力依赖性沉降导致肌动蛋白丝中的张力增加,从而激活MS Ca(2+) 通透通道,这可能是重力刺激导致Ca(2+)浓度增加的分子机制。我们回顾了使用先进生物物理方法研究肌动蛋白丝和MS通道张力感知的最新进展,并讨论了它们在重力感知中的可能作用。