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首页> 外文期刊>Journal of Experimental Botany >Carbon monoxide regulates the expression of the wound-inducible gene ipomoelin through antioxidation and MAPK phosphorylation in sweet potato
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Carbon monoxide regulates the expression of the wound-inducible gene ipomoelin through antioxidation and MAPK phosphorylation in sweet potato

机译：一氧化碳通过抗氧化作用和MAPK磷酸化作用来调节伤口诱导基因ipomoelin的表达

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摘要

Carbon monoxide (CO), one of the haem oxygenase (HO) products, plays important roles in plant development and stress adaptation. However, the function of CO involved in wounding responses is seldom studied. A wound-inducible gene, ipomoelin (IPO), of sweet potato (Ipomoea batatas cv. Tainung 57) was used as a target to study the regulation of CO in wounding responses. After wounding for 1 h, the endogenous CO content and IbHO expression level were significantly reduced in leaves. IPO expression upon wounding was prohibited by the HO activator hemin, whereas the HO inhibitor zinc protoporphyrin IX elevated IPO expression. The IPO expression induced by wounding, H2O2, or methyl jasmonate was inhibited by CO. CO also affected the activities of ascorbate peroxidase, catalase, and peroxidase, and largely decreased H2O2 content in leaves. CO inhibited the extracellular signal-regulated kinase (ERK) phosphorylation induced by wounding. IbMAPK, the ERK of sweet potato, was identified by immunoblotting, and the interaction with its upstream activator, IbMEK1, was further confirmed by bimolecular fluorescence complementation and co-immunoprecipitation. Conclusively, wounding in leaves repressed IbHO expression and CO production, induced H2O2 generation and ERK phosphorylation, and then stimulated IPO expression.
机译：一氧化碳（CO）是血红素加氧酶（HO）的产物之一，在植物发育和逆境适应中起着重要作用。然而，很少研究涉及伤口反应的CO的功能。甘薯（Ipomoea batatas cv。Tainung 57）的伤口诱导基因ipomoelin（IPO）被用作研究CO对伤口反应的调控的靶标。受伤1小时后，叶片内源性CO含量和IbHO表达水平明显降低。 HO激活剂血红素禁止受伤时IPO表达，而HO抑制剂锌原卟啉IX提高IPO表达。 CO可以抑制受伤，H2O2或茉莉酸甲酯诱导的IPO表达。CO还影响抗坏血酸过氧化物酶，过氧化氢酶和过氧化物酶的活性，并大大降低叶片中H2O2的含量。一氧化碳抑制受伤诱导的细胞外信号调节激酶（ERK）磷酸化。通过免疫印迹鉴定了IbMAPK（甘薯的ERK），并通过双分子荧光互补和共免疫沉淀进一步证实了其与上游激活剂IbMEK1的相互作用。结论是，叶片受伤可抑制IbHO表达和CO产生，诱导H2O2生成和ERK磷酸化，然后刺激IPO表达。

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