Constitutive activation of AtMEK5, a MAPK kinase, induces salicylic acid-independent cell death in Arabidopsis thaliana
Constitutive activation of AtMEK5, a MAPK kinase, induces salicylic acid-independent cell death in Arabidopsis thaliana
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AtMEK5（一种 MAPK 激酶）的组成型激活可诱导拟南芥中不依赖于水杨酸的细胞死亡
DOI：
10.1360/982004-280
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发表时间：
2004
影响因子：
--
通讯作者：
D. Ren
中科院分区：
文献类型：
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作者：
Hongxia Liu;Ying Wang;Tianhong Zhou;Yujing Sun;Guoqin Liu;D. Ren
AtMEK5DD是拟南芥中MAP激酶AtMEK5的活性突变体。在转基因植物中诱导AtMEK5DD表达导致44和48 kD MAPK的激活并导致细胞快速死亡。为了比较AtMEK5DD表达诱导的细胞死亡与无毒病原体感染诱导的HR细胞死亡，我们分析了永久性转基因拟南芥植物中下游MAP激酶的激活和PR基因表达的诱导。凝胶内激酶活性测定结果表明，携带Avr Rpt 2基因的假单胞菌DC3000感染后，44 kD和48 kD的MAPKs也被激活。在经历由P.erichingae DC 3000感染引起的HR细胞死亡的植物中，PAL、PR 1和PR 5被强烈诱导，而在表达AtMEK5DD蛋白的转基因植物中，仅PR 5的表达被强烈诱导。AtMEK5DD × NahG植株中的NahG蛋白不能抑制AtMEK5DD诱导的细胞死亡。而AtMEK5DD × NahG表达的AtMEK5DD植株中水杨酸（SA）含量无显著变化。所有这些都表明，AtMEK 5激活诱导的细胞死亡是水杨酸非依赖性的。
AtMEK5DD is an active mutant of AtMEK5, a MAP kinase kinase in Arabidopsis. Induction of AtMEK5DD expression in transgenic plants leads to activation of 44 and 48 kD MAPKs and causes a rapid cell death. To compare the cell death induced by the expression of AtMEK5DD with the HR-cell death induced by avirulence pathogen infection, we analyzed the activation of downstream MAP Kinase and induction of PR genes expression in permanent transgenic Arabidopsis plants. In-gel kinase activity assay revealed that the infection of Pseudomonas syringae DC3000 harboring Avr Rpt2 gene also lead to activation of 44 and 48 kD MAPKs. PAL, PR1 and PR5 were strongly induced in plants undergoing HR-cell death caused by the infection of P. syringae DC3000, while only the expression of PR5 was strongly induced in transgenic plants expressing AtMEK5DD protein. NahG protein in AtMEK5DD × NahG plants cannot suppress the cell death induced by AtMEK5DD. And AtMEK5DD protein expressed AtMEK5DD × NahG plants showed no significant change in salicylic acid (SA) level. All these suggest that the cell death induced by the activation of AtMEK5 is salicylic acid-independent.
影响因子：
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作者：
G. Pfeifer;A. Riggs
通讯作者：
G. Pfeifer;A. Riggs
影响因子：
11.6
作者：
Rogers, EE;Ausubel, FM
通讯作者：
Ausubel, FM