Abstract：
RADICAL-INDUCED CELL DEATH1 (RCD1) is an Arabidopsis thaliana nuclear protein that is disrupted during oxidative stress. RCD1 is considered an important integrative node in development and stress responses, and the rcd1 plants have several phenotypes and altered resistance to a variety of abiotic and biotic stresses. One of the phenotypes of rcd1 is resistance to the herbicide paraquat, but the mechanisms behind it are unknown. Paraquat causes a rapid burst of reactive oxygen species (ROS) initially in the chloroplast. We performed multi-platform metabolomic analyses in wild type Col-0 and paraquat resistant rcd1 plants to identify pathways conveying resistance and the function of RCD1 in this respect. Wild type and rcd1 plants were clearly distinguished by their abundance of antioxidants and specialized metabolites and their responses to paraquat. The lack of response in rcd1 suggested constitutively active defense against ROS via elevated flavonoid, glutathione, β-carotene, and tocopherol levels, whereas its ascorbic acid levels were compromised under non-stressed control conditions when compared to Col-0. We propose that RCD1 acts as a hub that maintains basal antioxidant system, and its inactivation induces defense responses by enhancing the biosynthesis and redox cycling of low molecular weight antioxidants and specialized metabolites with profound antioxidant activities alleviating oxidative stress.
摘要：
RADICAL诱导的细胞死亡1(RCD1)是一种在氧化应激过程中被破坏的拟南芥核蛋白。RCD1被认为是发育和应激反应的重要整合节点，rcd1植物具有几种表型，并且对各种非生物和生物胁迫的抗性发生了变化。rcd1的表型之一是对除草剂百草枯的抗性，但背后的机制是未知的。百草枯最初在叶绿体中引起活性氧（ROS）的快速爆发。我们在野生型Col-0和百草枯抗性rcd1植物中进行了多平台代谢组学分析，以鉴定传达抗性的途径和RCD1在这方面的功能。野生型和rcd1植物通过其丰富的抗氧化剂和专门的代谢产物以及对百草枯的反应而被清楚地区分开。rcd1缺乏响应表明通过升高的类黄酮对ROS的组成性积极防御，谷胱甘肽,β-胡萝卜素,和生育酚水平，而与Col-0相比，其抗坏血酸水平在非应激对照条件下受损。我们建议RCD1充当维持基础抗氧化系统的枢纽，它的失活通过增强低分子量抗氧化剂和具有丰富抗氧化活性的专门代谢产物的生物合成和氧化还原循环来诱导防御反应，从而减轻氧化应激。
