【摘要】 以Fluo-3AM为Ca²⁺荧光探针,结合激光共聚焦扫描显微技术,观察到在处理后数十秒内,气孔关闭之前,茉莉酸（JA）可引起[Ca²⁺]cyt的迅速上升;叶照和JA的前体物亚麻酸（LA）几乎不能引起[Ca²⁺]cyt的明显变化;钙的螯合剂EGTA预处理可完全阻断JA诱导气孔关闭的效应,并且JA不再引起保卫细胞[Ca²⁺]cyt增加;质膜Ca²⁺通道的抑制剂硝苯吡啶（nifedipine,NIF）可减弱JA诱导气孔关闭的效应,也使JA诱导保卫细胞[Ca²⁺]cyt增加的幅度有所下降;胞内Ca²⁺释放的抑制剂钌红不能明显改变JA诱导气孔关闭的趋势,但使JA引起的保卫细胞[Ca²⁺]cyt增加有所降低。实验结果表明:Ca²⁺参与JA诱导气孔关闭的信号转导;推测JA引起的[Ca²⁺]cyt升高可能主要来源于胞外,但不能完全排除胞内Ca²⁺的释放。更多还原

【Abstract】 Ca²⁺, an ubiquitous second messenger in the signal transudation pathway, is re- quired for various physiological and developmental processes in plant. Jasmonic acid （JA） has been known to induce the stomatal closure. By monitoring the changes of [Ca²⁺]_cyt with fluorescent probe Fluo-3 AM under the confocal microscopy, we observed that exogenous JA increased [Ca²⁺]_cyt in guard cells of Vicia faba L. while the control and linolenic acid （LA）, which is a precursor of JA, could hardly affect the change of [Ca²⁺]_cyt. EGTA, a chelator of Ca²⁺ completely blocked JA-in- duced stomatal closure. After epidermis pretreated with EGTA, JA failed to result in [Ca²⁺]_cyt in- creasing. Ruthenium red that blocked Ca²⁺ released from intracellular Ca²⁺ store could not signifi- cantly change JA-induced stomatal closure, while JA still increased [Ca²⁺]_cyt. Furthermore, Ca²⁺ channel inhibitor of nifedipine （NIF） reduced the effectiveness of JA-induced stomatal closure and JA-induced increasing fluorescent intensity in guard cells. The results demonstrated that Ca²⁺ is in- volved in the signal transduction of JA induced stomatal closure, and the source of [Ca²⁺]_cyt in- creasing in guard cells induced by JA might derive mainly from the external stores.更多还原