Mitochondrial VOLTAGE-DEPENDENT ANION CHANNEL 3 regulates stomatal closure by abscisic acid signaling

被引:4
作者
Qin, Haixia [1 ]
Yang, Wenqi [1 ]
Liu, Zile [1 ]
Ouyang, Yi [1 ]
Wang, Xiao [1 ]
Duan, Haiyang [2 ]
Zhao, Bing [1 ]
Wang, Shujie [1 ]
Zhang, Junli [1 ]
Chang, Yuankai [3 ]
Jiang, Kun [4 ]
Yu, Ke [1 ]
Zhang, Xuebin [1 ]
机构
[1] Henan Univ, Sch Life Sci, State Key Lab Crop Stress Adaptat & Improvement, Henan Joint Int Lab Crop Multiom Res, Kaifeng 475004, Peoples R China
[2] Henan Agr Univ, State Key Lab Wheat & Maize Crop Sci, Coll Agron, Zhengzhou 450002, Peoples R China
[3] Henan Univ, Sch Life Sci, Kaifeng 475004, Peoples R China
[4] Zhejiang Univ, Coll Life Sci, Hangzhou 310058, Peoples R China
关键词
ABA-INDEPENDENT INHIBITION; ACTIVATED PROTEIN-KINASES; HYDROGEN-PEROXIDE; SEED-GERMINATION; RECEPTOR KINASE; MOLECULAR-BASIS; ARABIDOPSIS; STRESS; INTERACTS; MEMBRANE;
D O I
10.1093/plphys/kiad516
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
In Arabidopsis (Arabidopsis thaliana), stomatal closure mediated by abscisic acid (ABA) is redundantly controlled by ABA receptor family proteins (PYRABACTIN RESISTANCE 1 [PYR1]/PYR1-LIKE [PYLs]) and subclass III SUCROSE NONFERMENTING 1 (SNF1)-RELATED PROTEIN KINASES 2 (SnRK2s). Among these proteins, the roles of PYR1, PYL2, and SnRK2.6 are more dominant. A recent discovery showed that ABA-induced accumulation of reactive oxygen species (ROS) in mitochondria promotes stomatal closure. By analyzing stomatal movements in an array of single and higher order mutants, we revealed that the mitochondrial protein VOLTAGE-DEPENDENT ANION CHANNEL 3 (VDAC3) jointly regulates ABA-mediated stomatal closure with a specialized set of PYLs and SnRK2s by affecting cellular and mitochondrial ROS accumulation. VDAC3 interacted with 9 PYLs and all 3 subclass III SnRK2s. Single mutation in VDAC3, PYLs (except PYR1 and PYL2), or SnRK2.2/2.3 had little effect on ABA-mediated stomatal closure. However, knocking out PYR1, PYL1/2/4/8, or SnRK2.2/2.3 in vdac3 mutants resulted in significantly delayed or attenuated ABA-mediated stomatal closure, despite the presence of other PYLs or SnRK2s conferring redundant functions. We found that cellular and mitochondrial accumulation of ROS induced by ABA was altered in vdac3pyl1 mutants. Moreover, H2O2 treatment restored ABA-induced stomatal closure in mutants with decreased stomatal sensitivity to ABA. Our work reveals that VDAC3 ensures redundant control of ABA-mediated stomatal closure by canonical ABA signaling components. Arabidopsis mitochondrial protein VOLTAGE-DEPENDENT ANION CHANNEL 3 regulates abscisic acid-mediated stomatal closure by affecting cellular and mitochondrial accumulation of reactive oxygen species.
引用
收藏
页码:1041 / 1058
页数:18
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