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The Arabidopsis Calcium-Dependent Protein Kinase, CPK6, Functions as a Positive Regulator of Methyl Jasmonate Signaling in Guard Cells1[W][OA]

机译:拟南芥钙依赖性蛋白激酶CPK6充当保护细胞中茉莉酸甲酯信号的正向调节剂[W] [OA]

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摘要

Previous studies have demonstrated that methyl jasmonate (MeJA) induces stomatal closure dependent on change of cytosolic free calcium concentration in guard cells. However, these molecular mechanisms of intracellular Ca2+ signal perception remain unknown. Calcium-dependent protein kinases (CDPKs) function as Ca2+ signal transducers in various plant physiological processes. It has been reported that four Arabidopsis (Arabidopsis thaliana) CDPKs, CPK3, CPK6, CPK4, and CPK11, are involved in abscisic acid signaling in guard cells. It is also known that there is an interaction between MeJA and abscisic acid signaling in guard cells. In this study, we examined the roles of these CDPKs in MeJA signaling in guard cells using Arabidopsis mutants disrupted in the CDPK genes. Disruption of the CPK6 gene impaired MeJA-induced stomatal closure, but disruption of the other CDPK genes did not. Despite the broad expression pattern of CPK6, we did not find other remarkable MeJA-insensitive phenotypes in the cpk6-1 mutant. The whole-cell patch-clamp analysis revealed that MeJA activation of nonselective Ca2+-permeable cation channels is impaired in the cpk6-1 mutant. Consistent with this result, MeJA-induced transient cytosolic free calcium concentration increments were reduced in the cpk6-1 mutant. MeJA failed to activate slow-type anion channels in the cpk6-1 guard cells. Production of early signal components, reactive oxygen species and nitric oxide, in guard cells was elicited by MeJA in the cpk6-1 mutant as in the wild type. These results provide genetic evidence that CPK6 has a different role from CPK3 and functions as a positive regulator of MeJA signaling in Arabidopsis guard cells.
机译:先前的研究表明,茉莉酸甲酯(MeJA)诱导气孔关闭,这取决于保卫细胞中胞质游离钙浓度的变化。但是,细胞内Ca 2+信号感知的这些分子机制仍然未知。钙依赖性蛋白激酶(CDPK)在多种植物生理过程中起Ca2 +信号转导的作用。据报道,四种拟南芥(拟南芥)CDPK,CPK3,CPK6,CPK4和CPK11与保卫细胞中的脱落酸信号有关。还已知在保卫细胞中MeJA和脱落酸信号传导之间存在相互作用。在这项研究中,我们使用在CDPK基因中破坏的拟南芥突变体,研究了这些CDPK在保卫细胞MeJA信号中的作用。 CPK6基因的破坏会损害MeJA诱导的气孔关闭,而其他CDPK基因的破坏则不会。尽管CPK6的表达模式广泛,我们在cpk6-1突变体中未发现其他明显的MeJA不敏感表型。全细胞膜片钳分析表明,在cpk6-1突变体中,非选择性Ca2 +渗透性阳离子通道的MeJA激活受到损害。与该结果一致,在cpk6-1突变体中,MeJA诱导的瞬时胞质游离钙浓度增加降低。 MeJA无法激活cpk6-1保护细胞中的慢型阴离子通道。与野生型一样,MeJA在cpk6-1突变体中诱导了保卫细胞中早期信号成分,活性氧和一氧化氮的产生。这些结果提供了遗传证据,表明CPK6与CPK3具有不同的作用,并在拟南芥保卫细胞中充当MeJA信号的正向调节剂。

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