【摘要】 ABA、H2O2和硝普钠(SNP)均能诱导蚕豆气孔 关闭。NO的清除剂c-PTIO可以减轻由ABA或H2O2所 诱导的蚕豆气孔关闭的程度,而过氧化氢酶(CAT)则不 能减轻NO诱导的气孔关闭程度。激光共聚焦显微检测 结果显示,10 μmol／L的ABA处理后,胞内H2O2的产 生速率明显高于NO的产生速率;CAT几乎可完全抑 制ABA所诱导的DAF的荧光增加;外源H2O2能显著 诱导胞内DAF的荧光增加;c-PTIO对ABA诱导的DCF 荧光略有促进作用,但外源SNP不能诱导胞内DCF荧 光增加。这些结果表明,在ABA诱导气孔关闭过程中, H2O2可能在NO的上游起作用并受NO的负反馈调节。更多还原

【Abstract】 It is usually suggested that either H2O2 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 H2O2 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 H2O2 signaling to mediate ABA-induced stomatal closure in Vicia faba L. Sodium nitroprusside (SNP, a NO donor) and H2O2 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 H2O2 (Fig.2), while catalase (CAT), a H2O2 scavenger, failed to reverse the NO-induced aperture reduction in Vicia faba guard cells (Fig.3). Monitoring the changes in both NO and H2O2 generation in guard cells by using fluorescent probe of NO or H2O2, DAF-2DA or H2DCFDA, respectively, we found that the generating rate of H2O2 in guard cells was faster than that of NO after being treated with ABA 10 μmol/L (Figs.4, 5). CAT almost completely inhibited the increase in DAF fluorescence induced by ABA (Fig.4). Similar to ABA, exogenous H2O2 provoked the production of NO (Fig.6). c-PTIO slightly enhanced the fluorescent intensity of DCF stimulated by ABA (Fig. 4), while exogenous SNP did not increase DCF fluorescence in guard cells (Fig.6). Taken together, these results suggest that H2O2 could probably act as upstream component of NO signaling and NO negatively regulate H2O2 generation during ABA-induced stomatal closure in guard cells.更多还原