Control of Volume and Turgor in Stomatal Guard Cells
Control of Volume and Turgor in Stomatal Guard Cells
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DOI：
10.1007/s00232-005-0851-7
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发表时间：
2006-07
期刊：
影响因子：
--
通讯作者：
E. Macrobbie
中科院分区：
文献类型：
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作者：
E. Macrobbie
植物的水分损失是由叶表皮气孔的孔径决定的，气孔的孔径由钾盐的液泡积累水平决定，因此一对保卫细胞的体积和膨压决定。离子通过液泡膜的通量调节是气孔开度调节的关键，而离子通过液泡膜的通量调节只能通过示踪剂通量测量来研究。液泡膜中有两个运输系统。第一个是Ca 2+激活的通道，被氧化苯胂（PAO）抑制，负责响应“干旱”激素脱落酸（阿坝）释放液泡K+（Rb+）。该通道对压力敏感，在低膨压时下调，在高膨压时上调，为膨压调节提供系统。阿坝诱导液泡离子流出的瞬时刺激，在此期间，通量跟踪离子含量（体积，膨压），这表明阿坝降低了控制系统的设定点。第二个系统，这是PAO不敏感的，是负责离子通量从液泡到细胞质与向内的水流后，低渗转移。有人建议，这涉及到一个水通道蛋白作为传感器，也许也作为响应;变形的水通道蛋白可能使其离子渗透性，或者，可替代地，变形的水通道蛋白可能向相关的离子通道发出信号，激活it. Treatment与抑制剂的水通道蛋白，氯化汞或银磺胺嘧啶，产生一个大的瞬时增加离子释放的液泡，也PAO不敏感。有人建议，这涉及到相同的水通道蛋白，无论是呈现直接离子渗透，或信号激活相关的离子通道。
Water loss from plants is determined by the aperture of stomatal pores in the leaf epidermis, set by the level of vacuolar accumulation of potassium salt, and hence volume and turgor, of a pair of guard cells. Regulation of ion fluxes across the tonoplast, the key to regulation of stomatal aperture, can only be studied by tracer flux measurements. There are two transport systems in the tonoplast. The first is a Ca2+-activated channel, inhibited by phenylarsine oxide (PAO), responsible for the release of vacuolar K+(Rb+) in response to the “drought” hormone, abscisic acid (ABA). This channel is sensitive to pressure, down-regulated at low turgor and up-regulated at high turgor, providing a system for turgor regulation. ABA induces a transient stimulation of vacuolar ion efflux, during which the flux tracks the ion content (volume, turgor), suggesting ABA reduces the set-point of a control system. The second system, which is PAO-insensitive, is responsible for an ion flux from vacuole to cytoplasm associated with inward water flow following a hypo-osmotic transfer. It is suggested that this involves an aquaporin as sensor, and perhaps also as responder; deformation of the aquaporin may render it ion-permeable, or, alternatively, the deformed aquaporin may signal to an associated ion channel, activating it. Treatment with inhibitors of aquaporins, HgCl2or silver sulfadiazine, produces a large transient increase in ion release from the vacuole, also PAO-insensitive. It is suggested that this involves the same aquaporin, either rendered directly ion-permeable, or signalling to activate an associated ion channel.