乙烯诱导的气孔关闭是通过 MKK1/3–MPK3/6 级联到 EIN2 和 EIN3 介导的,Journal of Integrative Plant Biology

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乙烯诱导的气孔关闭是通过 MKK1/3–MPK3/6 级联到 EIN2 和 EIN3 介导的
Journal of Integrative Plant Biology ( IF 9.3 ) Pub Date : 2021-02-19 , DOI: 10.1111/jipb.13083
Teng-Yue Zhang ₁ , Zhong-Qi Li ₁ , Yu-Dong Zhao ₁ , Wen-Jie Shen ₁ , Meng-Shu Chen ₁ , Hai-Quan Gao ₁ , Xiao-Min Ge ₁ , Hui-Qin Wang ₁ , Xue Li ₁ , Jun-Min He ₁

Affiliation

丝裂原活化蛋白激酶 (MPK) 在保卫细胞信号传导中起重要作用，但 MPK 级联反应是否参与保卫细胞乙烯信号传导并与过氧化氢 (H ₂ O ₂ )、一氧化氮 (NO) 和乙烯信号传导成分相互作用仍然存在不清楚。在这里，我们报告了乙烯激活野生型拟南芥叶片中的 MPK3 和 MPK6以及乙烯不敏感 2 ( ein2 )、ein3、硝酸还原酶 1 ( nia1 ) 和nia2突变体，但这种作用在乙烯反应 1 ( etr1 ), 烟酰胺腺嘌呤二核苷酸磷酸氧化酶AtrbohF , mpk 激酶1( mkk1 ) 和mkk3突变体。相比之下，组成型三重响应1 ( ctr1 ) 突变体具有组成型活性的 MPK3 和 MPK6。酵母双杂交、双分子荧光互补和下拉分析表明 MPK3 和 MPK6 与 MKK1、MKK3 和 EIN2 (EIN2 CEND) 的 C 端区域发生物理相互作用。mkk1、mkk3、mpk3和mpk6突变体具有典型水平的乙烯诱导的 H ₂ O ₂生成但削弱了乙烯诱导的 EIN2 CEND 切割和核易位、EIN3 蛋白积累、保卫细胞中的 NO 产生和气孔关闭。这些结果表明，MKK1/3–MPK3/6 级联通过在 ETR1、CTR1 和 H ₂ O ₂下游起作用与 EIN2 相互作用来介导乙烯诱导的气孔关闭，从而促进保卫细胞中 EIN3 的积累和 EIN3 依赖性 NO 的产生.

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Ethylene-induced stomatal closure is mediated via MKK1/3–MPK3/6 cascade to EIN2 and EIN3

Mitogen-activated protein kinases (MPKs) play essential roles in guard cell signaling, but whether MPK cascades participate in guard cell ethylene signaling and interact with hydrogen peroxide (H₂O₂), nitric oxide (NO), and ethylene-signaling components remain unclear. Here, we report that ethylene activated MPK3 and MPK6 in the leaves of wild-type Arabidopsis thaliana as well as ethylene insensitive2 (ein2), ein3, nitrate reductase1 (nia1), and nia2 mutants, but this effect was impaired in ethylene response1 (etr1), nicotinamide adenine dinucleotide phosphate oxidase AtrbohF, mpk kinase1 (mkk1), and mkk3 mutants. By contrast, the constitutive triple response1 (ctr1) mutant had constitutively active MPK3 and MPK6. Yeast two-hybrid, bimolecular fluorescence complementation, and pull-down assays indicated that MPK3 and MPK6 physically interacted with MKK1, MKK3, and the C-terminal region of EIN2 (EIN2 CEND). mkk1, mkk3, mpk3, and mpk6 mutants had typical levels of ethylene-induced H₂O₂ generation but impaired ethylene-induced EIN2 CEND cleavage and nuclear translocation, EIN3 protein accumulation, NO production in guard cells, and stomatal closure. These results show that the MKK1/3–MPK3/6 cascade mediates ethylene-induced stomatal closure by functioning downstream of ETR1, CTR1, and H₂O₂ to interact with EIN2, thereby promoting EIN3 accumulation and EIN3-dependent NO production in guard cells.

更新日期：2021-02-19

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