Department of Botany and Plant Biology, Section of Biology, Faculty of Sciences, University of Geneva, 1211 Geneva, Switzerland; email:
Institute of Genetics and Genomics of Geneva (iGE3), University of Geneva, 1211 Geneva, Switzerland.
Annu Rev Plant Biol. 2021 Jun 17;72:793-822. doi: 10.1146/annurev-arplant-050718-095946. Epub 2021 Feb 26.
Ultraviolet-B (UV-B) radiation is an intrinsic fraction of sunlight that plants perceive through the UVR8 photoreceptor. UVR8 is a homodimer in its ground state that monomerizes upon UV-B photon absorption via distinct tryptophan residues. Monomeric UVR8 competitively binds to the substrate binding site of COP1, thus inhibiting its E3 ubiquitin ligase activity against target proteins, which include transcriptional regulators such as HY5. The UVR8-COP1 interaction also leads to the destabilization of PIF bHLH factor family members. Additionally, UVR8 directly interacts with and inhibits the DNA binding of a different set of transcription factors. Each of these UVR8 signaling mechanisms initiates nuclear gene expression changes leading to UV-B-induced photomorphogenesis and acclimation. The two WD40-repeat proteins RUP1 and RUP2 provide negative feedback regulation and inactivate UVR8 by facilitating redimerization. Here, we review the molecular mechanisms of the UVR8 pathway from UV-B perception and signal transduction to gene expression changes and physiological UV-B responses.
紫外线-B（UV-B）辐射是阳光的固有组成部分，植物通过 UVR8 光受体感知到它。UVR8 在其基态下是一个同源二聚体，在吸收 UV-B 光子后通过独特的色氨酸残基单体化。单体 UVR8 竞争性地结合到 COP1 的底物结合位点，从而抑制其针对靶蛋白（包括 HY5 等转录调节剂）的 E3 泛素连接酶活性。UVR8-COP1 相互作用还导致 PIF bHLH 因子家族成员的不稳定。此外，UVR8 还直接相互作用并抑制另一组转录因子的 DNA 结合。这些 UVR8 信号传导机制中的每一种都启动核基因表达变化，导致 UV-B 诱导的光形态发生和适应。两种 WD40 重复蛋白 RUP1 和 RUP2 通过促进重二聚化提供负反馈调节并使 UVR8 失活。在这里，我们综述了 UVR8 途径从 UV-B 感知和信号转导到基因表达变化和生理 UV-B 反应的分子机制。
