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转录因子NAC075通过抑制活性氧积累延缓叶片衰老

Transcription Factor NAC075 Delays Leaf Senescence by Deterring Reactive Oxygen Species Accumulation in .

作者信息

Kan Chengcheng, Zhang Yi, Wang Hou-Ling, Shen Yingbai, Xia Xinli, Guo Hongwei, Li Zhonghai

机构信息

Beijing Advanced Innovation Center for Tree Breeding by Molecular Design, Beijing Forestry University, Beijing, China.

National Engineering Laboratory for Tree Breeding, College of Biological Sciences and Technology, Beijing Forestry University, Beijing, China.

出版信息

Front Plant Sci. 2021 Feb 24;12:634040. doi: 10.3389/fpls.2021.634040. eCollection 2021.

Abstract

Leaf senescence is a highly complex genetic process that is finely tuned by multiple layers of regulation. Among them, transcriptional regulation plays a critical role in controlling the initiation and progression of leaf senescence. Here, we found that the NAC transcription factor NAC075 functions as a novel negative regulator of leaf senescence. Loss of function of NAC075 promotes leaf senescence in an age-dependent manner, whereas constitutive overexpression of delays senescence in . Transcriptome analysis revealed that transcript levels of antioxidant enzymes such as catalase (CAT), ascorbate peroxidase (APX), and superoxide dismutase (SOD) are significantly suppressed in mutants compared with wild-type plants. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analyses revealed that NAC075 directly binds the promoter of (). Moreover, genetic analysis showed that overexpression of suppresses the overproduction of reactive oxygen species (ROS) and the early senescence phenotypes of mutants, suggesting that CAT2 acts downstream of NAC075 to delay leaf senescence by repressing ROS accumulation. Collectively, our findings provide a new regulatory module involving NAC075-CAT2-ROS in controlling leaf senescence in .

摘要

叶片衰老 是一个高度复杂的遗传过程,受到多层调控的精细调节。其中,转录调控在控制叶片衰老的起始和进程中起着关键作用。在这里,我们发现NAC转录因子NAC075作为叶片衰老的一种新型负调控因子发挥作用。NAC075功能缺失以年龄依赖性方式促进叶片衰老,而其组成型过表达则延迟了(此处原文缺失相关植物名称)的衰老。转录组分析表明,与野生型植物相比,(此处原文缺失相关植物名称)突变体中过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)和超氧化物歧化酶(SOD)等抗氧化酶的转录水平显著受到抑制。电泳迁移率变动分析(EMSA)和染色质免疫沉淀(ChIP)分析表明,NAC075直接结合(此处原文缺失相关基因名称)的启动子。此外,遗传分析表明,(此处原文缺失相关基因名称)的过表达抑制了活性氧(ROS)的过量产生和(此处原文缺失相关植物名称)突变体的早期衰老表型,这表明CAT2在NAC075下游发挥作用,通过抑制ROS积累来延迟叶片衰老。总的来说,我们的研究结果提供了一个新的调控模块,即NAC075 - CAT2 - ROS参与控制(此处原文缺失相关植物名称)的叶片衰老。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4449/7943619/974faf4e95a5/fpls-12-634040-g001.jpg

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