Abscisic acid increases hydrogen peroxide in mitochondria to facilitate stomatal closure.
Abscisic acid increases hydrogen peroxide in mitochondria to facilitate stomatal closure.
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DOI：
10.1093/plphys/kiac601
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发表时间：
2023-05-02
期刊：
影响因子：
7.4
通讯作者：
Muday, Gloria K.
中科院分区：
文献类型：
--
作者：
Postiglione, Anthony E.;Muday, Gloria K.
脱落酸(ABA)驱动气孔关闭，以最大限度地减少干旱时蒸腾作用造成的水分损失。我们研究了ABA在拟南芥保卫细胞中增加的ROS积累的亚细胞定位，保卫细胞驱动气孔关闭。在线粒体、叶绿体、胞浆和细胞核中观察到依赖于ABA的ROS感受器二氯荧光素(DCF)的荧光增强。在ABA不敏感的五重受体突变体中，所有这些位置的ABA反应都丢失了。与MitoTracker Red共定位的DCF-和H_2O_2选择性探针Peroxy Orange 1的线粒体中的ABA荧光增强。ABA处理以细胞质(roGFP2-Orp1)或线粒体(mt-roGFP2-Orp1)为靶点的遗传编码的过氧化氢报告基因转化的保卫细胞，显示出过氧化氢的增加。与线粒体ROS在气孔关闭中的功能变化一致，我们发现线粒体缺陷突变体ABA过度敏感6(上述6)的保卫细胞增加了ABA诱导的线粒体ROS，促进了气孔关闭。这些效应被鱼藤酮所抑制，鱼藤酮增加了线粒体的ROS。相反，线粒体靶向抗氧化剂MitoQ抑制了ABA对Col-0线粒体ROS积累和气孔关闭的影响，并逆转了上述6个突变体的保卫细胞关闭表型。在编码呼吸爆发氧化酶同源酶(RBOH)酶基因的突变体中，ABA诱导的ROS积累在保卫细胞线粒体中消失，并被RBOH抑制剂VAS2870处理减少，这与RBOH作用于ABA增加保卫细胞线粒体ROS的机制一致。这些结果表明，ABA促进保卫细胞线粒体中H_2O_2的积累，从而促进气孔关闭。
Abscisic acid (ABA) drives stomatal closure to minimize water loss due to transpiration in response to drought. We examined the subcellular location of ABA-increased accumulation of reactive oxygen species (ROS) in guard cells, which drive stomatal closure, in Arabidopsis (Arabidopsis thaliana). ABA-dependent increases in fluorescence of the generic ROS sensor, dichlorofluorescein (DCF), were observed in mitochondria, chloroplasts, cytosol, and nuclei. The ABA response in all these locations was lost in an ABA-insensitive quintuple receptor mutant. The ABA-increased fluorescence in mitochondria of both DCF- and an H2O2-selective probe, Peroxy Orange 1, colocalized with Mitotracker Red. ABA treatment of guard cells transformed with the genetically encoded H2O2 reporter targeted to the cytoplasm (roGFP2-Orp1), or mitochondria (mt-roGFP2-Orp1), revealed H2O2 increases. Consistent with mitochondrial ROS changes functioning in stomatal closure, we found that guard cells of a mutant with mitochondrial defects, ABA overly sensitive 6 (abo6), have elevated ABA-induced ROS in mitochondria and enhanced stomatal closure. These effects were phenocopied with rotenone, which increased mitochondrial ROS. In contrast, the mitochondrially targeted antioxidant, MitoQ, dampened ABA effects on mitochondrial ROS accumulation and stomatal closure in Col-0 and reversed the guard cell closure phenotype of the abo6 mutant. ABA-induced ROS accumulation in guard cell mitochondria was lost in mutants in genes encoding respiratory burst oxidase homolog (RBOH) enzymes and reduced by treatment with the RBOH inhibitor, VAS2870, consistent with RBOH machinery acting in ABA-increased ROS in guard cell mitochondria. These results demonstrate that ABA elevates H2O2 accumulation in guard cell mitochondria to promote stomatal closure.
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影响因子：
7.4
作者：
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通讯作者：
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10.1073/pnas.0912021106
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影响因子：
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