Phosphorylation of the plasma membrane H+-ATPase AHA2 by BAK1 is required for ABA-induced stomatal closure in Arabidopsis
Phosphorylation of the plasma membrane H+-ATPase AHA2 by BAK1 is required for ABA-induced stomatal closure in Arabidopsis
复制标题
BAK1 磷酸化质膜 H -ATP 酶 AHA2 是 ABA 诱导拟南芥气孔关闭所必需的
DOI：
10.1093/plcell/koac106
复制
发表时间：
2022-06-23
期刊：
影响因子：
11.6
通讯作者：
Gong, Zhizhong
中科院分区：
文献类型：
--
作者：
Pei, Dan;Hua, Deping;Gong, Zhizhong
在干旱胁迫下，光激活质膜质子ATP酶（PM H+-ATP酶）主要促进气孔的开放，而脱落酸（阿坝）信号主要调控气孔的关闭。PM H+-ATP酶是否参与ABA诱导的气孔关闭尚不清楚。我们确定BRI 1相关受体激酶1（BAK 1）与主要的PM拟南芥H+-ATP酶亚型2（AHA 2）相互作用，磷酸化并激活。来自aha 2 -6单突变体拟南芥植物的离体叶片损失与bak 1 -4单突变体和aha 2 -6 bak 1 -4双突变体一样多的水，所有三种突变体比野生型（哥伦比亚-0 [Col-0]）损失更多的水。与这些观察结果一致，aha 2 -6，bak 1 -4，和aha 2 -6 bak 1 -4突变体不太敏感ABA诱导的气孔关闭比Col-0，而aha 2 -6突变不影响ABA抑制气孔开放在光照条件下。ABA激活的BAK 1磷酸化AHA 2的C-末端的Ser-944，并激活AHA 2，导致快速的H+外流，细胞质碱化和活性氧（ROS）的积累，启动阿坝信号转导和气孔关闭。由自身启动子驱动的磷酸化模拟突变体AHA 2（S944 D）可以在很大程度上补偿aha 2 -6和bak 1 -4突变体中的失水、细胞质碱化和ROS积累的缺陷表型。研究结果揭示了AHA 2在干旱胁迫下细胞质碱化和ABA诱导的气孔关闭中的重要作用，BAK 1磷酸化的AHA 2在拟南芥细胞质碱化和活性氧积累的上游正向调节ABA诱导的气孔关闭。
Stomatal opening is largely promoted by light-activated plasma membrane-localized proton ATPases (PM H+-ATPases), while their closure is mainly modulated by abscisic acid (ABA) signaling during drought stress. It is unknown whether PM H+-ATPases participate in ABA-induced stomatal closure. We established that BRI1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) interacts with, phosphorylates and activates the major PM Arabidopsis H+-ATPase isoform 2 (AHA2). Detached leaves from aha2-6 single mutant Arabidopsis thaliana plants lost as much water as bak1-4 single and aha2-6 bak1-4 double mutants, with all three mutants losing more water than the wild-type (Columbia-0 [Col-0]). In agreement with these observations, aha2-6, bak1-4, and aha2-6 bak1-4 mutants were less sensitive to ABA-induced stomatal closure than Col-0, whereas the aha2-6 mutation did not affect ABA-inhibited stomatal opening under light conditions. ABA-activated BAK1 phosphorylated AHA2 at Ser-944 in its C-terminus and activated AHA2, leading to rapid H+ efflux, cytoplasmic alkalinization, and reactive oxygen species (ROS) accumulation, to initiate ABA signal transduction and stomatal closure. The phosphorylation-mimicking mutation AHA2(S944D) driven by its own promoter could largely compensate for the defective phenotypes of water loss, cytoplasmic alkalinization, and ROS accumulation in both aha2-6 and bak1-4 mutants. Our results uncover a crucial role of AHA2 in cytoplasmic alkalinization and ABA-induced stomatal closure during the plant's response to drought stress.AHA2 phosphorylated by BAK1 positively regulates ABA-induced stomatal closure upstream of cytoplasmic alkalinization and ROS accumulation in Arabidopsis.