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乙烯通过抑制叶黄素循环来调控拟南芥中依赖能量的非光化学猝灭。

Ethylene Regulates Energy-Dependent Non-Photochemical Quenching in Arabidopsis through Repression of the Xanthophyll Cycle.

作者信息

Chen Zhong, Gallie Daniel R

机构信息

Department of Biochemistry, University of California, Riverside, California, United States of America.

出版信息

PLoS One. 2015 Dec 2;10(12):e0144209. doi: 10.1371/journal.pone.0144209. eCollection 2015.

DOI:10.1371/journal.pone.0144209
PMID:26630486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4667945/
Abstract

Energy-dependent (qE) non-photochemical quenching (NPQ) thermally dissipates excess absorbed light energy as a protective mechanism to prevent the over reduction of photosystem II and the generation of reactive oxygen species (ROS). The xanthophyll cycle, induced when the level of absorbed light energy exceeds the capacity of photochemistry, contributes to qE. In this work, we show that ethylene regulates the xanthophyll cycle in Arabidopsis. Analysis of eto1-1, exhibiting increased ethylene production, and ctr1-3, exhibiting constitutive ethylene response, revealed defects in NPQ resulting from impaired de-epoxidation of violaxanthin by violaxanthin de-epoxidase (VDE) encoded by NPQ1. Elevated ethylene signaling reduced the level of active VDE through decreased NPQ1 promoter activity and impaired VDE activation resulting from a lower transthylakoid membrane pH gradient. Increasing the concentration of CO2 partially corrected the ethylene-mediated defects in NPQ and photosynthesis, indicating that changes in ethylene signaling affect stromal CO2 solubility. Increasing VDE expression in eto1-1 and ctr1-3 restored light-activated de-epoxidation and qE, reduced superoxide production and reduced photoinhibition. Restoring VDE activity significantly reversed the small growth phenotype of eto1-1 and ctr1-3 without altering ethylene production or ethylene responses. Our results demonstrate that ethylene increases ROS production and photosensitivity in response to high light and the associated reduced plant stature is partially reversed by increasing VDE activity.

摘要

能量依赖型(qE)非光化学猝灭(NPQ)通过热耗散过量吸收的光能,作为一种保护机制,以防止光系统II过度还原以及活性氧(ROS)的产生。当吸收的光能水平超过光化学能力时诱导的叶黄素循环有助于qE。在这项工作中,我们表明乙烯调节拟南芥中的叶黄素循环。对乙烯产量增加的eto1-1和组成型乙烯反应的ctr1-3进行分析,发现NPQ1编码的紫黄质脱环氧化酶(VDE)对紫黄质的脱环氧化受损导致NPQ出现缺陷。升高的乙烯信号通过降低NPQ1启动子活性和由于较低的类囊体膜pH梯度导致的VDE激活受损,降低了活性VDE的水平。增加CO2浓度部分纠正了乙烯介导的NPQ和光合作用缺陷,表明乙烯信号的变化影响基质中CO2的溶解度。在eto1-1和ctr1-3中增加VDE表达恢复了光激活的脱环氧化和qE,减少了超氧化物的产生并减少了光抑制。恢复VDE活性显著逆转了eto1-1和ctr1-3的矮小生长表型,而不改变乙烯产量或乙烯反应。我们的结果表明,乙烯在高光响应下增加ROS产生和光敏感性,并且通过增加VDE活性部分逆转了相关的植株矮小现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/088b/4667945/5fd476534a5f/pone.0144209.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/088b/4667945/485f2e9331b7/pone.0144209.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/088b/4667945/c12e7528f18d/pone.0144209.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/088b/4667945/5fd476534a5f/pone.0144209.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/088b/4667945/485f2e9331b7/pone.0144209.g001.jpg
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