NO可能作为H2O2的下游信号介导ABA诱导的蚕豆气孔关闭

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,10μmo1/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.

NO May Function in the Downstream of H2O2 in ABA-induced Stomatal Closure in Vicia faba L.

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.