摘要
以Fluo-3AM为Ca^(2+)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[Ca^(2+)]cyt的迅速上升;叶照和JA的前体物亚麻酸(LA)几乎不能引起[Ca^(2+)]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[Ca^(2+)]cyt增加;质膜Ca^(2+)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[Ca^(2+)]cyt增加的幅度有所下降;胞内Ca^(2+)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[Ca^(2+)]cyt增加有所降低。实验结果表明:Ca^(2+)参与JA诱导气孔关闭的信号转导;推测JA引起的[Ca^(2+)]cyt升高可能主要来源于胞外,但不能完全排除胞内Ca^(2+)的释放。
Ca^2＋, an ubiquitous second messenger in the signal transudation pathway, is required for various physiological and developmental processes in plant. Jasmonic acid （JA） has been known to induce the stomatal closure. By monitoring the changes of [Ca^2＋]cyt with fluorescent probe Fluo-3 AM under the confocal microscopy, we observed that exogenous JA increased [Ca^2＋]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 [Ca^2＋]cyt,. EGTA, a chelator of Ca^2＋ completely blocked JA-induced stomatal closure. After epidermis pretreated with EGTA, JA failed to result in [Ca^2＋]cyt, increasing. Ruthenium red that blocked Ca^2＋ released from intracellular Ca^2＋ store could not significantly change JA-induced stomatal closure, while JA still increased [Ca^2＋]cyt. Furthermore, Ca^2＋ 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 Ca^2＋ is involved in the signal transduction of JA induced stomatal closure, and the source of [Ca^2＋]cyt, increasing in guard cells induced by JA might derive mainly from the external stores.
出处
《实验生物学报》
CSCD
北大核心
2005年第4期297-302,共6页
Acta Biologiae Experimentalis Sinica
基金
国家自然科学基金(批准号:30370141)
高等学校博士点基金(批准号:20020019018)
山东省教育厅基金(批准号:J04C13)
