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以及在叶片衰老年龄调控中的作用。

and Function in Age Gating of Leaf Senescence.

作者信息

Xie Yurong, Ma Mengdi, Liu Yang, Wang Baobao, Wei Hongbin, Kong Dexin, Wang Haiyang

机构信息

Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing, China.

State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, South China Agricultural University, Guangzhou, China.

出版信息

Front Plant Sci. 2021 Oct 28;12:770060. doi: 10.3389/fpls.2021.770060. eCollection 2021.

DOI:10.3389/fpls.2021.770060
PMID:34777451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8584998/
Abstract

Leaf senescence is the terminal stage of leaf development. Both light and the plant hormone ethylene play important roles in regulating leaf senescence. However, how they coordinately regulate leaf senescence during leaf development remains largely unclear. In this study, we show that FHY3 and FAR1, two homologous proteins essential for phytochrome A-mediated light signaling, physically interact with and repress the DNA binding activity of EIN3 (a key transcription factor essential for ethylene signaling) and PIF5 (a bHLH transcription factor negatively regulating light signaling), and interfere with their DNA binding to the promoter of , which encodes a key NAC transcription factor promoting leaf senescence. In addition, we show that FHY3, PIF5, and EIN3 form a tri-protein complex(es) and that they coordinately regulate the progression of leaf senescence. We show that during aging or under dark conditions, accumulation of FHY3 protein decreases, thus lifting its repression on DNA binding of EIN3 and PIF5, leading to the increase of expression and onset of leaf senescence. Our combined results suggest that FHY3 and FAR1 act in an age gating mechanism to prevent precocious leaf senescence by integrating light and ethylene signaling with developmental aging.

摘要

叶片衰老为叶片发育的末期阶段。光照与植物激素乙烯在调控叶片衰老过程中均发挥重要作用。然而,在叶片发育过程中它们如何协同调控叶片衰老仍很大程度上不清楚。在本研究中,我们发现FHY3和FAR1这两个对光敏色素A介导的光信号传导至关重要的同源蛋白,与EIN3(乙烯信号传导关键转录因子)和PIF5(负调控光信号传导的bHLH转录因子)发生物理相互作用并抑制其DNA结合活性,且干扰它们与编码促进叶片衰老关键NAC转录因子的启动子的DNA结合。此外,我们发现FHY3、PIF5和EIN3形成三蛋白复合体,且它们协同调控叶片衰老进程。我们表明在衰老期间或黑暗条件下,FHY3蛋白积累减少,从而解除其对EIN3和PIF5 DNA结合的抑制,导致表达增加和叶片衰老开始。我们的综合结果表明,FHY3和FAR1通过将光和乙烯信号与发育衰老整合,在年龄调控机制中发挥作用以防止叶片早衰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/97f8e1b02fca/fpls-12-770060-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/0ad2ca0dd625/fpls-12-770060-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/705ce7cc678f/fpls-12-770060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/c17659ff9b51/fpls-12-770060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/c29e7553845f/fpls-12-770060-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/96827db058ca/fpls-12-770060-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/cfc12e663c0c/fpls-12-770060-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/97f8e1b02fca/fpls-12-770060-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/0ad2ca0dd625/fpls-12-770060-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/705ce7cc678f/fpls-12-770060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/c17659ff9b51/fpls-12-770060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/c29e7553845f/fpls-12-770060-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/96827db058ca/fpls-12-770060-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/cfc12e663c0c/fpls-12-770060-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb8f/8584998/97f8e1b02fca/fpls-12-770060-g007.jpg

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