首页 | 本学科首页   官方微博 | 高级检索  
   检索      

Ca^2+参与茉莉酸诱导蚕豆气孔关闭的信号转导
引用本文:刘新,石武良,张蜀秋,娄成后.Ca^2+参与茉莉酸诱导蚕豆气孔关闭的信号转导[J].实验生物学报,2005,38(4):297-302.
作者姓名:刘新  石武良  张蜀秋  娄成后
作者单位:[1]中国农业大学生物学院植物生理学与生物化学国家重点实验室,北京100094 [2]莱阳农学院生命科学学院,青岛266109
基金项目: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)和山东省教育厅基金(批准号:J04C13)资助.
摘    要:以Fluo-3 AM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;对照和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Cah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诱导气孔关闲的趋势,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。

关 键 词:钙离子  茉莉酸  蚕豆  气孔关闭  信号转导  保卫细胞  胞质  诱导抗病性
收稿时间:2004-11-15
修稿时间:2004-11-15

CALCIUM INVOLVED IN THE SIGNALING PATHWAY OF JASMONIC ACID INDUCED STOMATAL CLOSURE OF VICIA FABA L.
Liu Xin;Dan WuLiang;Zhang ShuQiu;Lou ChengHou.CALCIUM INVOLVED IN THE SIGNALING PATHWAY OF JASMONIC ACID INDUCED STOMATAL CLOSURE OF VICIA FABA L.[J].Acta Biologiae Experimentalis Sinica,2005,38(4):297-302.
Authors:Liu Xin;Dan WuLiang;Zhang ShuQiu;Lou ChengHou
Institution:State Key Lab of Plant Physiol. Biochem. College of Biological Sciences,China Agricultural University, Beijing.
Abstract:Ca2+, 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 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-induced stomatal closure. After epidermis pretreated with EGTA, JA failed to result in Ca2+]cyt increasing. Ruthenium red that blocked Ca2+ released from intracellular Ca2+ store could not significantly 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 involved in the signal transduction of JA induced stomatal closure, and the source of Ca2+]cyt increasing in guard cells induced by JA might derive mainly from the external stores.
Keywords:
本文献已被 维普 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号