2018年2月2日，Developmental Cell杂志在线发表了中国科学院上海生命科学研究院植物生理生态研究所刘宏涛研究组题为“UVR8 Interacts with BES1 and BIM1 to Regulate Transcription and Photomorphogenesis in Arabidopsis”的研究论文，文章揭示了紫外光UV-B与内源油菜素甾醇信号协同调控生长的新机制。

已知UV-B光抑制植物生长，但其机理尚不清楚。UVR8是植物中介导UV-B光反应的UV-B光受体。本文中，UV-B通过抑制科院促进植物植物生长的BR信号来抑制植物生长。UVR8与功能性去磷酸化的BES1和转录因子BIM1在物理上相互作用，介导BR调节的基因表达和植物生长以抑制其活性。全基因组基因表达分析，鉴定了依赖BES1的，UV-B调控的转录组，其中富含与细胞延伸和植物生长有关的基因。进一步的结果表明，UVB激活和细胞核定位的UVR8抑制BES1/BIM1的DNA结合活性，直接调节生长相关基因的转录。因此，我们的研究结果表明，UVR8-BES1/BIM1相互作用代表了植物早期的光受体信号传导机制，并且是整合光和BR信号的重要模块。

UV-B light (UV-B radiation) is known to inhibit plant growth, but the mechanism is not well understood. UVR8 (UV RESISTANCE LOCUS 8) is a UV-B light photoreceptor that mediates UV-B light responses in plants. We report here that UV-B inhibits plant growth by repressing plant steroid hormone brassinosteroid (BR)-promoted plant growth. UVR8 physically interacts with the functional dephosphorylated BES1 (BRI1-EMS-SUPPRESSOR1) and BIM1 (BES1-INTERACTING MYC-LIKE 1) transcription factors that mediate BR-regulated gene expression and plant growth to inhibit their activities. Genome-wide gene expression analysis defined a BES1-dependent UV-B-regulated transcriptome, which is enriched with genes involved in cell elongation and plant growth. We further showed that UV-B-activated and nucleus-localized UVR8 inhibited the DNA-binding activities of BES1/BIM1 to directly regulate transcription of growth-related genes. Our results therefore establish that UVR8-BES1/BIM1 interaction represents an early photoreceptor signaling mechanism in plants and serves as an important module integrating light and BR signaling.