UV-B light is a potential stress factor in plants, but how plants coordinate growth and UV-B stress responses is not well understood. Here, we report that brassinosteroid (BR) signaling inhibits UV-B stress responses in Arabidopsis (Arabidopsis thaliana) and various crops by controlling flavonol biosynthesis. We further demonstrate that BRI1-EMS-SUPPRESSOR 1 (BES1) mediates the tradeoff between plant growth and UV-B defense responses. BES1, a master transcription factor involved in BR signaling, represses the expression of transcription factor genes MYB11, MYB12, and MYB111, which activate flavonol biosynthesis. BES1 directly binds to the promoters of these MYBs in a BR-enhanced manner to repress their expression, thereby reducing flavonol accumulation. However, exposure to broadband UV-B down-regulates BES1 expression, thus promoting flavonol accumulation. These findings demonstrate that BR-activated BES1 not only promotes growth but also inhibits flavonoid biosynthesis. UV-B stress suppresses the expression of BES1 to allocate energy to flavonoid biosynthesis and UV-B stress responses, allowing plants to switch from growth to UV-B stress responses in a timely manner.

UV-B 光是植物的潜在胁迫因素，但植物如何协调生长和 UV-B 胁迫反应尚不清楚。在这里，我们报道油菜素类固醇 (BR) 信号通过控制黄酮醇生物合成来抑制拟南芥 ( Arabidopsis thaliana ) 和各种作物的 UV-B 胁迫反应。我们进一步证明 BRI1-EMS-SUPPRESSOR 1 (BES1) 介导植物生长和 UV-B 防御反应之间的权衡。 BES1 是参与 BR 信号传导的主转录因子，抑制转录因子基因MYB11 、 MYB12和MYB111的表达，从而激活黄酮醇生物合成。 BES1以BR增强的方式直接结合这些MYB的启动子来抑制它们的表达，从而减少黄酮醇的积累。然而，暴露于宽带 UV-B 下会下调BES1表达，从而促进黄酮醇积累。这些发现表明，BR 激活的 BES1 不仅能促进生长，还能抑制类黄酮生物合成。 UV-B胁迫抑制BES1的表达，为类黄酮生物合成和UV-B胁迫反应分配能量，使植物及时从生长转向UV-B胁迫反应。