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HY5-HDA9 Module Transcriptionally Regulates Plant Autophagy in Response to Light-to-Dark Conversion and Nitrogen Starvation.
Molecular Plant ( IF 27.5 ) Pub Date : 2020-02-19 , DOI: 10.1016/j.molp.2020.02.011
Chao Yang 1 , Wenjin Shen 1 , Lianming Yang 1 , Yun Sun 1 , Xibao Li 1 , Minyi Lai 1 , Juan Wei 1 , Chaojun Wang 2 , Yingchao Xu 3 , Faqiang Li 4 , Shan Liang 1 , Chengwei Yang 1 , Shangwei Zhong 5 , Ming Luo 6 , Caiji Gao 1
Affiliation  

Light is arguably one of the most important environmental factors that determines virtually all aspects of plant growth and development, but the molecular link between light signaling and the autophagy pathway has not been elucidated in plants. In this study, we demonstrate that autophagy is activated during light-to-dark conversion though transcriptional upregulation of autophagy-related genes (ATGs). We showed that depletion of the ELONGATED HYPOCOTYL 5 (HY5), a key component of light signaling, leads to enhanced autophagy activity and resistance to extended darkness and nitrogen starvation treatments, contributing to higher expression of ATGs. HY5 interacts with and recruits HISTONE DEACETYLASE 9 (HDA9) to ATG5 and ATG8e loci to repress their expression by deacetylation of the Lys9 and Lys27 of histone 3. Furthermore, we found that both darkness and nitrogen depletion induce the degradation of HY5 via 26S proteasome and the concomitant disassociation of HDA9 from ATG5 and ATG8e loci, leading to their depression and thereby activated autophagy. Genetic analysis further confirmed that HY5 and HDA9 act synergistically and function upstream of the autophagy pathway. Collectively, our study unveils a previously unknown transcriptional and epigenetic network that regulates autophagy in response to light-to-dark conversion and nitrogen starvation in plants.



中文翻译:

HY5-HDA9 模块转录调节植物自噬以响应光到暗的转换和氮饥饿。

光可以说是决定植物生长和发育的几乎所有方面的最重要的环境因素之一,但光信号与自噬途径之间的分子联系在植物中尚未阐明。在这项研究中,我们通过自噬相关基因 ( ATG )的转录上调证明了自噬在从光到暗的转换过程中被激活。我们发现,光信号的关键成分 ELONGATED HYPOCOTYL 5 (HY5) 的消耗会导致自噬活性增强以及对延长黑暗和氮饥饿治疗的抵抗力,从而导致ATG s 的更高表达。HY5 与组蛋白去乙酰化酶 9 (HDA9) 相互作用并将其募集到ATG5ATG8e基因座通过组蛋白 3 的 Lys9 和 Lys27 的去乙酰化来抑制它们的表达。此外,我们发现黑暗和氮消耗都通过 26S 蛋白酶体诱导 HY5 的降解,并伴随着 HDA9 从ATG5ATG8e基因座解离,导致它们的抑郁从而激活自噬。遗传分析进一步证实了 HY5 和 HDA9 协同作用并在自噬途径上游发挥作用。总的来说,我们的研究揭示了一个以前未知的转录和表观遗传网络,该网络调节自噬以响应植物中的光到暗转换和氮饥饿。

更新日期:2020-02-19
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