REVERSIBLE INACTIVATION OF K+ CHANNELS OF VICIA STOMATAL GUARD-CELLS FOLLOWING THE PHOTOLYSIS OF CAGED INOSITOL 1,4,5-TRISPHOSPHATE
REVERSIBLE INACTIVATION OF K+ CHANNELS OF VICIA STOMATAL GUARD-CELLS FOLLOWING THE PHOTOLYSIS OF CAGED INOSITOL 1,4,5-TRISPHOSPHATE
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DOI：
10.1038/346766a0
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发表时间：
1990-08-23
期刊：
影响因子：
64.8
通讯作者：
TRENTHAM, DR
中科院分区：
文献类型：
--
作者：
BLATT, MR;THIEL, G;TRENTHAM, DR
最近的研究表明，细胞质D-肌肌醇1，4，5-三磷酸（InsP 3）的功能作为第二信使在植物中，在动物中，耦合环境和其他刺激细胞内Ca 2+释放1，2。InsP 3的细胞质水平和植物中几种可能的前体的周转受到生理刺激的影响，包括光，渗透胁迫和植物激素吲哚乙酸3 -5-和InsP 3激活Ca 2+通道6和Ca 2+通量通过植物液泡7和微粒体膜8。补充数据也链接细胞质游离钙的变化几个生理反应，特别是在保卫细胞调节气体交换通过气孔高等植物叶片。最近的证据表明，保卫细胞的K+通道，因此，气孔运动的K+流量9可能是由细胞质Ca 2+控制（参考文献10）。然而，到目前为止，InsP 3在植物信号转导中的作用的直接证据仍然难以捉摸。在这里，我们报告说，从无活性、光不稳定的前体InsP 3（笼状InsP 3）11的P5 - 1-（2-硝基苯基）乙酯释放的InsP 3可逆地灭活了K+通道，该通道被认为介导蚕豆保卫细胞对K+的吸收。同时激活一个明显与时间无关的内向电流，以降低膜电位并促进K+通过第二类K+通道流出12，13。这些数据与胞质游离Ca 2+的瞬时升高一致（参考文献9），并证明完整的保卫细胞能够在控制通过K+通道的离子通量的信号级联中使用InsP 3。
RECENT investigations suggest that cytoplasmic D-myo-inositol 1,4,5-trisphosphate (InsP3) functions as a second messenger in plants, as in animals, coupling environmental and other stimuli to intracellular Ca2+release1,2. Cytoplasmic levels of InsP3and the turnover of several probable precursors in plants are affected by physiological stimuli—including light, osmotic stress and the phytohormone indoleacetic acid3–5—and InsP3activates Ca2+channels6and Ca2+flux across plant vacuolar7and microsomal membranes8. Complementary data also link changes in cytoplasmic free Ca2+to several physiological responses, notably in guard cells which regulate gas exchange through the stomatal pores of higher plant leaves. Recent evidence indicates that guard cell K+channels and, hence, K+flux for stomatal movements9may be controlled by cytoplasmic Ca2+(ref. 10). So far, however, direct evidence of a role for InsP3in signalling in plants has remained elusive. Here we report that InsP3released from an inactive, photolabile precursor, theP5-l-(2-nitrophenyl)ethyl ester of InsP3(caged InsP3)11reversibly inactivates K+channels thought to mediate K+uptake by guard cells fromVicia fabaL. while simultaneously activating an apparently time-independent, inward current to depolarize the membrane potential and promote K+efflux through a second class of K+channels12,13. The data are consistent with a transient rise in cytoplasmic free Ca2+(ref. 9) and demonstrate that intact guard cells are competent to use InsP3in signal cascades controlling ion flux through K+channels.