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两种 E3 连接酶在. 中拮抗调控 UV-B 响应。

Two E3 ligases antagonistically regulate the UV-B response in .

机构信息

State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, 361102 Xiamen, China.

State Key Laboratory of Protein and Plant Gene Research, Peking-Tsinghua Center for Life Sciences, School of Advanced Agricultural Sciences and School of Life Sciences, Peking University, 100871 Beijing, China.

出版信息

Proc Natl Acad Sci U S A. 2019 Mar 5;116(10):4722-4731. doi: 10.1073/pnas.1816268116. Epub 2019 Feb 20.

DOI:10.1073/pnas.1816268116
PMID:30787186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6410811/
Abstract

Photomorphogenesis is a pivotal developmental strategy used by plants to respond to environmental light levels. During emergence from the soil and the establishment of photomorphogenesis, seedlings encounter increasing levels of UV-B irradiation and develop adaptive responses accordingly. However, the molecular mechanisms that orchestrate UV-B signaling cascades remain elusive. Here, we provide biochemical and genetic evidence that the prolonged signaling circuits of UV-B-induced photomorphogenesis involve two sets of E3 ligases and a transcription factor in The UV-B-inducible protein RUP1/RUP2 associates with the CUL4-DDB1 scaffold to form an E3 ligase, which represses photomorphogenesis by mediating the degradation of HY5, the hub transcription factor in the light signaling pathway. Conversely, COP1 directly targets RUP1/RUP2 for ubiquitination and degradation, leading to balanced RUP1/RUP2 accumulation, alleviation of the COP1-HY5 interaction, and stabilization of HY5 protein. Therefore, our study reveals that these two E3-substrate modules, CUL4-DDB1-RUP1/RUP2-HY5 and COP1-RUP1/RUP2, constitute the repression and derepression machinery by which plants respond to prolonged UV-B irradiation in photomorphogenic development.

摘要

光形态建成是植物对环境光水平做出响应的关键发育策略。在破土而出并建立光形态建成的过程中,幼苗会遇到不断增加的 UV-B 辐射,并相应地发展出适应性反应。然而,协调 UV-B 信号级联的分子机制仍不清楚。在这里,我们提供了生化和遗传证据,表明 UV-B 诱导的光形态建成的延长信号通路涉及两组 E3 连接酶和一个转录因子。UV-B 诱导的蛋白 RUP1/RUP2 与 CUL4-DDB1 支架结合形成 E3 连接酶,通过介导光信号通路中枢纽转录因子 HY5 的降解来抑制光形态建成。相反,COP1 直接将 RUP1/RUP2 作为泛素化和降解的靶标,导致 RUP1/RUP2 的平衡积累,减轻 COP1-HY5 相互作用,并稳定 HY5 蛋白。因此,我们的研究揭示了这两个 E3-底物模块,CUL4-DDB1-RUP1/RUP2-HY5 和 COP1-RUP1/RUP2,构成了植物在光形态建成发育中对长时间 UV-B 照射做出响应的抑制和去抑制机制。

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本文引用的文献

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Dual-Source Nuclear Monomers of UV-B Light Receptor Direct Photomorphogenesis in Arabidopsis.紫外线B光受体的双源核单体直接调控拟南芥的光形态建成
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