Shan Changjuan, Sun Haili
Henan Institute of Science and Technology, Xinxiang, 453003, China.
Collaborative Innovation Center of Modern Biological Breeding, Xinxiang, Henan Province, 453003, China.
Protoplasma. 2018 May;255(3):977-983. doi: 10.1007/s00709-017-1183-z. Epub 2017 Nov 14.
This study investigated the relationship between MEK1/2 and nitric oxide (NO) in jasmonic acid (JA)-regulated metabolism of ascorbate and glutathione in maize leaves. The results showed that JA increased the activities of APX, GR, MDHAR, DHAR, GalLDH, and γ-ECS; the contents of AsA and GSH; and the production of NO. Above increases except for γ-ECS activity and NO production were all suppressed by pre-treatments with MEK1/2 inhibitors PD98059 and U0126. Above increases were all suppressed by pre-treatments with nitric oxide synthase (NOS) inhibitor L-NAME and NO scavenger cPTIO. The results of western blot showed that JA enhanced the phosphorylation level of MEK1/2. Pre-treatments with L-NAME and cPTIO suppressed JA-induced phosphorylation level of MEK1/2. Our results suggested that JA-induced NO activated MEK1/2 by increasing the phosphorylation level, which, in turn, resulted in the upregulation of ascorbate and glutathione metabolism in maize leaves.
本研究调查了在茉莉酸(JA)调节的玉米叶片抗坏血酸和谷胱甘肽代谢中,MEK1/2与一氧化氮(NO)之间的关系。结果表明,JA提高了抗坏血酸过氧化物酶(APX)、谷胱甘肽还原酶(GR)、单脱氢抗坏血酸还原酶(MDHAR)、脱氢抗坏血酸还原酶(DHAR)、半乳糖脱氢酶(GalLDH)和γ-谷氨酰半胱氨酸合成酶(γ-ECS)的活性;抗坏血酸(AsA)和谷胱甘肽(GSH)的含量;以及NO的产生。除γ-ECS活性和NO产生外,上述增加均被MEK1/2抑制剂PD98059和U0126预处理所抑制。上述增加均被一氧化氮合酶(NOS)抑制剂L-NAME和NO清除剂cPTIO预处理所抑制。蛋白质免疫印迹结果表明,JA增强了MEK1/2的磷酸化水平。L-NAME和cPTIO预处理抑制了JA诱导的MEK1/2磷酸化水平。我们的结果表明,JA诱导的NO通过增加磷酸化水平激活MEK1/2,进而导致玉米叶片中抗坏血酸和谷胱甘肽代谢上调。