Different environmental conditions can lead plants to a condition termed oxidative stress, which is characterized by a disruption in the equilibrium between the production of reactive oxygen species (ROS) and antioxidant defenses. Glutathione peroxidase (GPX), an enzyme that acts as a peroxide scavenger in different organisms, has been identified as an important component in the signaling pathway during the developmental process and in stress responses in plants and yeast. Here, we demonstrate that the mitochondrial isoform of rice (Oryza sativa L. ssp. Japonica cv. Nipponbare) OsGPX3 is induced after treatment with the phytohormone abscisic acid (ABA) and is involved in its responses and in epigenetic modifications. Plants that have been silenced for OsGPX3 (gpx3i) present substantial changes in the accumulation of proteins related to these processes. These plants also have several altered ABA responses, such as germination, ROS accumulation, stomatal closure, and dark-induced senescence. This study is the first to demonstrate that OsGPX3 plays a role in ABA signaling and corroborate that redox homeostasis enzymes can act in different and complex pathways in plant cells.

Significance

This work proposes the mitochondrial glutathione peroxidase (OsGPX3) as a novel ABA regulatory pathway component. Our results suggest that this antioxidant enzyme is involved in ABA-responses, highlighting the complex pathways that these proteins can participate beyond the regulation of cellular redox status.

中文翻译：

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线粒体异构体谷胱甘肽过氧化物酶 3 (OsGPX3) 参与水稻植物的 ABA 反应

不同的环境条件会导致植物处于一种称为氧化应激的状态，其特征是活性氧 (ROS) 的产生和抗氧化防御之间的平衡被破坏。谷胱甘肽过氧化物酶 (GPX) 是一种在不同生物体中充当过氧化物清除剂的酶，已被确定为植物和酵母发育过程中信号通路和应激反应中的重要组成部分。在这里，我们证明水稻（Oryza sativa L. ssp. Japonica cv. Nipponbare）的线粒体异构体OsGPX3在用植物激素脱落酸 (ABA) 处理后被诱导，并参与其反应和表观遗传修饰。OsGPX3沉默的植物( gpx3i ) 呈现与这些过程相关的蛋白质积累的重大变化。这些植物还具有几种改变的 ABA 反应，例如发芽、ROS 积累、气孔关闭和黑暗诱导的衰老。本研究首次证明OsGPX3在 ABA 信号传导中发挥作用，并证实氧化还原稳态酶可以在植物细胞中以不同且复杂的途径发挥作用。

意义

这项工作提出了线粒体谷胱甘肽过氧化物酶 ( OsGPX3 ) 作为一种新的 ABA 调节途径成分。我们的研究结果表明，这种抗氧化酶参与了 ABA 反应，突出了这些蛋白质可以参与的复杂途径，超出了细胞氧化还原状态的调节。