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首页> 外文期刊>Plant biology >Two guard cell mitogen-activated protein kinases, MPK9 and MPK12, function in methyl jasmonate-induced stomatal closure in Arabidopsis thaliana
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Two guard cell mitogen-activated protein kinases, MPK9 and MPK12, function in methyl jasmonate-induced stomatal closure in Arabidopsis thaliana

机译:两种保卫细胞有丝分裂原激活的蛋白激酶MPK9和MPK12在茉莉酸甲酯诱导的拟南芥气孔关闭中起作用

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摘要

Methyl jasmonate (MeJA) and abscisic acid (ABA) signalling cascades share several signalling components in guard cells. We previously showed that two guard cell-preferential mitogen-activated protein kinases (MAPKs), MPK9 and MPK12, positively regulate ABA signalling in Arabidopsis thaliana. In this study, we examined whether these two MAP kinases function in MeJA signalling using genetic mutants for MPK9 and MPK12 combined with a pharmacological approach. MeJA induced stomatal closure in mpk9-1 and mpk12-1 single mutants as well as wild-type plants, but not in mpk9-1 mpk12-1 double mutants. Consistently, the MAPKK inhibitor PD98059 inhibited the MeJA-induced stomatal closure in wild-type plants. MeJA elicited reactive oxygen species (ROS) production and cytosolic alkalisation in guard cells of the mpk9-1, mpk12-1 and mpk9-1 mpk12-1 mutants, as well in wild-type plants. Furthermore, MeJA triggered elevation of cytosolic Ca2+ concentration ([Ca2+](cyt)) in the mpk9-1 mpk12-1 double mutant as well as wild-type plants. Activation of S-type anion channels by MeJA was impaired in mpk9-1 mpk12-1. Together, these results indicate that MPK9 and MPK12 function upstream of S-type anion channel activation and downstream of ROS production, cytosolic alkalisation and [Ca2+](cyt) elevation in guard cell MeJA signalling, suggesting that MPK9 and MPK12 are key regulators mediating both ABA and MeJA signalling in guard cells.
机译:茉莉酸甲酯(MeJA)和脱落酸(ABA)信号级联在保卫细胞中共享多个信号成分。我们以前显示,两个守卫细胞优先的促分裂原激活蛋白激酶(MAPK),MPK9和MPK12,正调控拟南芥中的ABA信号传导。在这项研究中,我们使用药理学方法结合MPK9和MPK12的基因突变,研究了这两个MAP激酶是否在MeJA信号中起作用。 MeJA在mpk9-1和mpk12-1单突变体以及野生型植物中诱导了气孔关闭,但在mpk9-1 mpk12-1双突变体中却没有。一致地,MAPKK抑制剂PD98059抑制了MeJA诱导的野生型植物的气孔关闭。 MeJA在mpk9-1,mpk12-1和mpk9-1 mpk12-1突变体以及野生型植物的保卫细胞中引起活性氧(ROS)产生和胞质碱化。此外,MeJA触发了mpk9-1 mpk12-1双重突变体以及野生型植物中胞质Ca2 +浓度([Ca2 +](cyt))的升高。在mpk9-1 mpk12-1中,MeJA对S型阴离子通道的激活受到损害。总之,这些结果表明MPK9和MPK12在S型阴离子通道激活的上游,ROS生成,胞质碱化和[Ca2 +](cyt)升高的下游在保卫细胞MeJA信号中起作用,表明MPK9和MPK12是介导两者的关键调控因子保卫细胞中的ABA和MeJA信号传导。

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