拟南芥和茄子中BIC-UVR8介导的紫外线-B响应抑制机制的功能保守性研究

Abstract

Maintaining cellular photosensitivity while preventing damage from excessive light energy is a crucial challenge for plants, and negative feedback inhibition of photoreceptors plays a vital role in achieving this balance. Here, we uncover a regulatory mechanism involved in the UVR8-mediated UV-B signalling pathway. Through a combination of genetic, biochemical and cross-species analyses, we identified Arabidopsis BIC1 and BIC2, along with their orthologs in eggplant ( Solanum melongena L.), as functionally conserved negative regulators in UV-B signalling. Through physical association with UVR8, BIC proteins likely stabilise its inactive dimeric state, which in turn attenuates UV‑B‑triggered monomerization and downstream transcriptional activation of the photoreceptor. Overexpression of BIC proteins in both eggplant and Arabidopsis promote hypocotyl elongation under UV-B, while the bic1bic2 double mutant exhibits enhanced photomorphogenesis. Notably, the uvr8-6bic1bic2 triple mutant displays an intermediate phenotype between the uvr8-6 and bic1bic2 parents, revealing a mutual regulatory relationship: BIC proteins inhibit UVR8 activity at the protein level, while UVR8 promotes BIC transcription via HY5. Heterologous overexpression of eggplant SmBIC proteins in Arabidopsis phenocopies the elongated hypocotyl phenotype of Arabidopsis BIC-overexpressors, further supporting functional conservation. Mechanistically, BICs attenuate UVR8-dependent transcriptional activation of HY5 without directly binding to the HY5 promoter. We establish a self-regulatory negative feedback loop in which HY5 activates BIC expression upon UV-B exposure, and BICs reciprocally suppress UVR8-mediated HY5 transactivation by stabilising the UVR8 dimer. This non-proteolytic regulatory circuit enables precise fine-tuning of photomorphogenic responses to fluctuating UV-B environments. Our study expands the functional repertoire of BIC proteins beyond blue light signalling and defines a conserved mec