[NO may function in the downstream of H2O2 in ABA-induced stomatal closure in Vicia faba L].
[NO may function in the downstream of H2O2 in ABA-induced stomatal closure in Vicia faba L].
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发表时间：
2005-02
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通讯作者：
Dong Lü;Xiao Zhang;Jing Jiang;G. An;Ling-Rui Zhang;Chunpeng Song
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作者：
Dong Lü;Xiao Zhang;Jing Jiang;G. An;Ling-Rui Zhang;Chunpeng Song
通常认为，H(2)O(2)或NO作为信号分子介导ABA诱导的保护细胞气孔关闭，但在ABA信号转导通路中，H(2)O(2)与NO之间的关系尚未见报道。本研究利用气孔分析和激光扫描共聚焦显微镜技术，首次发现NO作为H(2)O(2)信号的下游中间体，介导ABA诱导的蚕豆气孔关闭。硝普钠（SNP， NO供体）和H(2)O(2)可以模拟ABA对气孔关闭的影响。羧基ptio （c-PTIO）是一种特殊的NO清除剂，能部分逆转ABA或H(2)O(2)诱导的气孔关闭，而过氧化氢酶（CAT）是一种H(2)O(2)清除剂，不能逆转NO诱导的蚕豆保护细胞气孔缩小。利用NO或H(2)O(2)、DAF-2DA或H2DCFDA荧光探针分别监测保护细胞中NO和H(2)O(2)生成的变化，发现在ABA处理10微mol/L后，保护细胞中H(2)O(2)的生成速度比NO的生成速度快。CAT几乎完全抑制了ABA诱导的DAF荧光的增加。与ABA类似，外源的H(2)O(2)刺激了NO的产生。c-PTIO轻微增强了ABA刺激DCF的荧光强度，而外源SNP对保护细胞的DCF荧光没有增强作用。综上所述，这些结果表明，H(2)O(2)可能作为NO信号的上游组分，而在aba诱导的保护细胞气孔关闭过程中，NO负调控H(2)O(2)的产生。
It is usually suggested that either H(2)O(2) or NO function as a signal molecule in mediating the ABA-induced stomatal closure of guard cells, but there has been no report on the relationship between H(2)O(2) and NO in ABA signal transduction pathway. Here, using stomatal analysis and laser scanning cofocal microscope techniques, we show firstly that NO functions as a downstream intermediate of H(2)O(2) signaling to mediate ABA-induced stomatal closure in Vicia faba L. Sodium nitroprusside (SNP, a NO donor) and H(2)O(2) can mimic the effects of ABA on stomatal closure. Carboxy-PTIO (c-PTIO, a specific scavenger of NO) partly reverse the stomatal closure induced by ABA or H(2)O(2), while catalase (CAT), a H(2)O(2) scavenger, failed to reverse the NO-induced aperture reduction in Vicia faba guard cells. Monitoring the changes in both NO and H(2)O(2) generation in guard cells by using fluorescent probe of NO or H(2)O(2), DAF-2DA or H2DCFDA, respectively, we found that the generating rate of H(2)O(2) in guard cells was faster than that of NO after being treated with ABA 10 micromol/L. CAT almost completely inhibited the increase in DAF fluorescence induced by ABA. Similar to ABA, exogenous H(2)O(2) provoked the production of NO. c-PTIO slightly enhanced the fluorescent intensity of DCF stimulated by ABA, while exogenous SNP did not increase DCF fluorescence in guard cells. Taken together, these results suggest that H(2)O(2) could probably act as upstream component of NO signaling and NO negatively regulate H(2)O(2) generation during ABA-induced stomatal closure in guard cells.