Knockout of AtMKK1 enhances salt tolerance and modifies metabolic activities in Arabidopsis.
Knockout of AtMKK1 enhances salt tolerance and modifies metabolic activities in Arabidopsis.
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DOI：
10.4161/psb.24206
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发表时间：
2013-05
影响因子：
2.9
通讯作者：
Xing T
中科院分区：
文献类型：
--
作者：
Conroy C;Ching J;Gao Y;Wang X;Rampitsch C;Xing T
丝裂原活化蛋白激酶（MAPK）是植物生长发育的重要调控机制。响应变化的条件而快速激活和阻断MAPK途径的能力有助于植物适应变化的环境。AtMKK 1是一种应激反应激酶，能够激活MAPK蛋白AtMPK 3、AtMPK 4和AtMPK 6。为了进一步阐明其作用模式，进行了几项试验，以检查AtMKK 1的敲除（KO）突变体的AtMKK 1盐胁迫的反应。我们发现AtMKK 1突变体植物在发芽和成年期都能耐受高水平的盐。蛋白质组学分析表明，AtMKK 1基因敲除突变体在高盐胁迫下线粒体H+-ATP酶α亚基、线粒体NADH脱氢酶和线粒体甲酸脱氢酶的表达水平升高。通过免疫印迹和酶测定进一步证实了甲酸脱氢酶的水平。这些酶在耐盐性的可能参与进行了讨论。
Mitogen-activated protein kinase (MAPK) pathways represent a crucial regulatory mechanism in plant development. The ability to activate and inactivate MAPK pathways rapidly in response to changing conditions helps plants to adapt to a changing environment. AtMKK1 is a stress response kinase that is capable of activating the MAPK proteins AtMPK3, AtMPK4 and AtMPK6. To elucidate its mode of action further, several tests were undertaken to examine the response of AtMKK1 to salt stress using a knockout (KO) mutant of AtMKK1. We found that AtMKK1 mutant plants tolerated elevated levels of salt during both germination and adulthood. Proteomic analysis indicated that the level of the α subunit of mitochrondrial H+-ATPase, mitochrondial NADH dehydrogenase and mitochrondrial formate dehydrogenase was enhanced in AtMKK1 knockout mutants upon high salinity stress. The level of formate dehydrogenase was further confirmed by immunoblotting and enzyme assay. The possible involvement of these enzymes in salt tolerance is discussed.