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CONSTITUTIVELY PHOTOMORPHOGENIC1 promotes ABA-mediated inhibition of post-germination seedling establishment.组成型光形态建成 1 促进 ABA 介导的萌发后幼苗建立的抑制。
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COP1 通过介导 ABA 诱导的 ABI5 积累正向调控黑暗中拟南芥幼苗生长中的 ABA 信号。

COP1 positively regulates ABA signaling during Arabidopsis seedling growth in darkness by mediating ABA-induced ABI5 accumulation.

机构信息

State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China.

State Key Laboratory of Crop Stress Adaptation and Improvement, Collaborative Innovation Center of Crop Stress Biology, Henan University, Kaifeng 475004, China.

出版信息

Plant Cell. 2022 May 24;34(6):2286-2308. doi: 10.1093/plcell/koac073.

DOI:10.1093/plcell/koac073
PMID:35263433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9134052/
Abstract

CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1), a well-characterized E3 ubiquitin ligase, is a central repressor of seedling photomorphogenic development in darkness. However, whether COP1 is involved in modulating abscisic acid (ABA) signaling in darkness remains largely obscure. Here, we report that COP1 is a positive regulator of ABA signaling during Arabidopsis seedling growth in the dark. COP1 mediates ABA-induced accumulation of ABI5, a transcription factor playing a key role in ABA signaling, through transcriptional and post-translational regulatory mechanisms. We further show that COP1 physically interacts with ABA-hypersensitive DCAF1 (ABD1), a substrate receptor of the CUL4-DDB1 E3 ligase targeting ABI5 for degradation. Accordingly, COP1 directly ubiquitinates ABD1 in vitro, and negatively regulates ABD1 protein abundance in vivo in the dark but not in the light. Therefore, COP1 promotes ABI5 protein stability post-translationally in darkness by destabilizing ABD1 in response to ABA. Interestingly, we reveal that ABA induces the nuclear accumulation of COP1 in darkness, thus enhancing its activity in propagating the ABA signal. Together, our study uncovers that COP1 modulates ABA signaling during seedling growth in darkness by mediating ABA-induced ABI5 accumulation, demonstrating that plants adjust their ABA signaling mechanisms according to their light environment.

摘要

组成型光形态建成 1(COP1)是一种特征明确的 E3 泛素连接酶,是黑暗中幼苗光形态建成发育的主要抑制因子。然而,COP1 是否参与调节黑暗中脱落酸(ABA)信号仍很大程度上不清楚。在这里,我们报告 COP1 是黑暗中拟南芥幼苗生长过程中 ABA 信号的正调节剂。COP1 通过转录和翻译后调控机制介导 ABA 诱导的 ABI5 积累,ABI5 是 ABA 信号中起关键作用的转录因子。我们进一步表明,COP1 与 ABA 超敏 DCAF1(ABD1)物理相互作用,ABD1 是 CUL4-DDB1 E3 连接酶的底物受体,靶向 ABI5 进行降解。因此,COP1 在体外直接泛素化 ABD1,并在黑暗中而不是在光照下负调控体内 ABD1 蛋白丰度。因此,COP1 通过响应 ABA 使 ABD1 不稳定,从而在黑暗中促进 ABI5 蛋白的翻译后稳定性。有趣的是,我们揭示 ABA 在黑暗中诱导 COP1 的核积累,从而增强其传播 ABA 信号的活性。总之,我们的研究揭示了 COP1 通过介导 ABA 诱导的 ABI5 积累来调节黑暗中幼苗生长过程中的 ABA 信号,表明植物根据其光照环境来调整其 ABA 信号机制。