Department of Botany and Plant Biology, Section of Biology, Faculty of Sciences, University of Geneva, CH-1211, Geneva 4, Switzerland.
Institute of Genetics and Genomics of Geneva (iGE3), University of Geneva, Geneva, Switzerland.
Plant J. 2022 Jul;111(2):422-439. doi: 10.1111/tpj.15806. Epub 2022 May 27.
Plants undergo photomorphogenic development in the presence of light. Photomorphogenesis is repressed by the E3 ubiquitin ligase CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1), which binds to substrates through their valine-proline (VP) motifs. The UV RESISTANCE LOCUS 8 (UVR8) photoreceptor senses UV-B and inhibits COP1 through the cooperative binding of its own VP motif and photosensing core to COP1, thereby preventing COP1 binding to substrates, including the basic leucine zipper (bZIP) transcriptional regulator ELONGATED HYPOCOTYL 5 (HY5). As a key promoter of visible light and UV-B photomorphogenesis, HY5 requires coregulators for its function. The B-box family transcription factors BBX20-BBX22 were recently described as HY5 rate-limiting coactivators under red light, but their role in UVR8 signaling was unknown. Here we describe a hypermorphic bbx21-3D mutant with enhanced photomorphogenesis, carrying a proline-to-leucine mutation at position 314 in the VP motif that impairs the interaction with and regulation by COP1. We show that BBX21 and BBX22 are UVR8-dependently stabilized after UV-B exposure, which is counteracted by a repressor induced by HY5/BBX activity. bbx20 bbx21 bbx22 mutants under UV-B are impaired in hypocotyl growth inhibition, photoprotective pigment accumulation and the expression of several HY5-dependent genes under continuous UV-B, but the immediate induction of marker genes after exposure to UV-B remains surprisingly rather unaffected. We conclude that BBX20-BBX22 contribute to HY5 activity in a subset of UV-B responses, but that additional, presently unknown, coactivators for HY5 are functional in early UVR8 signaling.
植物在光照下进行光形态建成发育。光形态建成受到 E3 泛素连接酶 CONSTITUTIVELY PHOTOMORPHOGENIC 1（COP1）的抑制，COP1 通过其缬氨酸-脯氨酸（VP）基序与底物结合。UV 抵抗 LOCUS 8（UVR8）光受体感知 UV-B，并通过其自身 VP 基序和光传感核心与 COP1 的协同结合来抑制 COP1，从而防止 COP1 与包括碱性亮氨酸拉链（bZIP）转录调节剂 ELONGATED HYPOCOTYL 5（HY5）在内的底物结合。作为可见光和 UV-B 光形态建成的关键促进剂，HY5 需要共激活因子来发挥其功能。最近，B-box 家族转录因子 BBX20-BBX22 被描述为红光下 HY5 的限速共激活因子，但它们在 UVR8 信号中的作用尚不清楚。在这里，我们描述了一个具有增强光形态建成的超突变体 bbx21-3D，该突变体在 VP 基序的第 314 位发生脯氨酸到亮氨酸的突变，从而削弱了与 COP1 的相互作用和调节。我们表明，UV-B 暴露后 BBX21 和 BBX22 依赖于 UVR8 而稳定，而 HY5/BBX 活性诱导的抑制剂则抵消了这种稳定作用。在 UV-B 下，bbx20bbx21bbx22 突变体在抑制下胚轴生长、积累光保护色素和表达 HY5 依赖的基因方面受损，但在暴露于 UV-B 后立即诱导标记基因的表达仍然令人惊讶地几乎没有受到影响。我们得出结论，BBX20-BBX22 为 HY5 在 UV-B 响应的一部分中发挥作用，但 HY5 的其他、目前未知的共激活因子在早期 UVR8 信号中具有功能。
