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ZmMPK5 is required for the NADPH oxidase-mediated self-propagation of apoplastic H2O2 in brassinosteroid-induced antioxidant defence in leaves of maize

机译:ZmMPK5是NADPH氧化酶介导的质外性H2O2在玉米油菜素甾体诱导的玉米叶片抗氧化防御中的自我繁殖所必需的

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摘要

Brassinosteroids (BRs) have been shown to induce hydrogen peroxide (H2O2) accumulation, and BR-induced H2O2 up-regulates antioxidant defence systems in plants. However, the mechanisms by which BR-induced H2O2 regulates antioxidant defence systems in plants remain to be determined. In the present study, the role of ZmMPK5, a mitogen-activated protein kinase, in BR-induced anitioxidant defence and the relationship between the activation of ZmMPK5 and H2O2 production in BR signalling were investigated in leaves of maize (Zea mays) plants. BR treatment activated ZmMPK5, induced apoplastic and chloroplastic H2O2 accumulation, and enhanced the total activities of antioxidant enzymes. Such enhancements were blocked by pre-treatment with mitogen-activated protein kinase kinase (MAPKK) inhibitors and H2O2 inhibitors or scavengers. Pre-treatment with MAPKK inhibitors substantially arrested the BR-induced apoplastic H2O2 production after 6 h of BR treatment, but did not affect the levels of apoplastic H2O2 within 1 h of BR treatment. BR-induced gene expression of NADPH oxidase was also blocked by pre-treatment with MAPKK inhibitors and an apoplastic H2O2 inhibitor or scavenger after 120 min of BR treatment, but was not affected within 30 min of BR treatment. These results suggest that the BR-induced initial apoplastic H2O2 production activates ZmMPK5, which is involved in self-propagation of apoplastic H2O2 via regulation of NADPH oxidase gene expression in BR-induced antioxidant defence systems.
机译:已显示,油菜素类固醇(BRs)会诱导过氧化氢(H2O2)积累,并且BR诱导的H2O2上调植物的抗氧化防御系统。然而,BR诱导的H2O2调节植物抗氧化防御系统的机制仍有待确定。在本研究中,研究了玉米(Zea mays)植物叶片中丝裂原活化蛋白激酶ZmMPK5在BR诱导的抗氧化防御中的作用以及BR信号中ZmMPK5的活化与H2O2产生之间的关系。 BR处理激活了ZmMPK5,诱导了质外和叶绿体H2O2的积累,并增强了抗氧化酶的总活性。通过用促分裂原活化的蛋白激酶激酶(MAPKK)抑制剂和H2O2抑制剂或清除剂进行预处理,可以阻止此类增强。用MAPKK抑制剂预处理可在BR治疗6小时后基本阻止BR诱导的质外性H2O2的产生,但在BR治疗1小时内不影响质性过氧化氢的水平。在BR处理120分钟后,MAPMAP抑制剂和质外性过氧化氢抑制剂或清除剂对BR诱导的NADPH氧化酶基因表达也进行了阻断,但在BR处理30分钟内未受到影响。这些结果表明,BR诱导的最初质外体H2O2的产生激活了ZmMPK5,ZmMPK5通过调节BR诱导的抗氧化剂防御系统中NADPH氧化酶基因的表达而参与了质外性H2O2的自我繁殖。

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