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百草枯耐受性的代谢物谱分析——抗氧化防御机制的一种介质()

Metabolite Profiling of Paraquat Tolerant ()-A Mediator of Antioxidant Defence Mechanisms.

作者信息

Sipari Nina, Lihavainen Jenna, Keinänen Markku

机构信息

Viikki Metabolomics Unit, Organismal and Evolutionary Biology Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, P.O. Box 65, FI-00014 Helsinki, Finland.

Department of Environmental and Biological Sciences, University of Eastern Finland, P.O. Box 111, FI-80101 Joensuu, Finland.

出版信息

Antioxidants (Basel). 2022 Oct 15;11(10):2034. doi: 10.3390/antiox11102034.

Abstract

RADICAL-INDUCED CELL DEATH1 (RCD1) is an nuclear protein that is disrupted during oxidative stress. RCD1 is considered an important integrative node in development and stress responses, and the plants have several phenotypes and altered resistance to a variety of abiotic and biotic stresses. One of the phenotypes of 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 plants to identify pathways conveying resistance and the function of RCD1 in this respect. Wild type and plants were clearly distinguished by their abundance of antioxidants and specialized metabolites and their responses to paraquat. The lack of response in 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

自由基诱导的细胞死亡1(RCD1)是一种在氧化应激期间被破坏的核蛋白。RCD1被认为是发育和应激反应中的一个重要整合节点,植物具有多种表型,并改变了对各种非生物和生物胁迫的抗性。其中一种表型是对除草剂百草枯具有抗性,但其背后的机制尚不清楚。百草枯最初会在叶绿体中引发活性氧(ROS)的快速爆发。我们对野生型Col-0和抗百草枯的植物进行了多平台代谢组学分析,以确定传递抗性的途径以及RCD1在这方面的功能。野生型和植物通过其抗氧化剂和特殊代谢物的丰度以及它们对百草枯的反应而明显区分开来。植物缺乏反应表明,通过提高类黄酮、谷胱甘肽、β-胡萝卜素和生育酚水平,对ROS具有组成型活性防御,而与Col-0相比,在非胁迫对照条件下其抗坏血酸水平受到损害。我们提出,RCD1作为一个枢纽维持基础抗氧化系统,其失活通过增强低分子量抗氧化剂和具有深刻抗氧化活性的特殊代谢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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbb8/9598866/fbb4054b5b13/antioxidants-11-02034-g001.jpg

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