• Greening of cotyledons during de‐etiolation is critical for harvesting light energy and sustaining plant growth. PIF3 and HY5 antagonistically regulate protochlorophyllide synthesis in the dark. However, the mechanism by which the PIF3/HY5 module regulates genes involved in protochlorophyllide synthesis is not clear.
• Using genetic, molecular and biochemical techniques we identified that the B‐BOX protein BBX11 acts directly downstream of PIF3 and HY5 to transcriptionally modulate genes involved in protochlorophyllide synthesis.
• Dark‐grown bbx11 and 35S:BBX11 seedlings exhibit an enhanced and reduced ability to green, respectively, when exposed to light. Transcript levels of HEMA1 and CHLH are upregulated in 35S:BBX11 seedlings that accumulate high levels of protochlorophyllide in the dark and undergo photobleaching upon illumination. PIF3 inhibits BBX11 in the dark by directly binding to its promoter. bbx11 suppresses the cotyledon greening defect of pif3 after prolonged dark, indicating that the PIF3‐mediated regulation of greening is dependent on BBX11. The enhanced greening of hy5 is also suppressed in hy5 lines overexpressing BBX11. In light, HY5 directly binds to the promoter of BBX11 and activates its expression to regulate BBX11‐mediated hypocotyl inhibition.
• We show that a PIF3/HY5 module regulates BBX11 expression in opposite ways to optimise protochlorophyllide accumulation in the dark and promote photomorphogenesis in light.

中文翻译：

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PIF3 / HY5模块调节BBX11，以在黑暗中抑制原叶绿素水平并在光照下促进光形态发生

• 脱去异黄酮期间子叶的绿化对于收获光能和维持植物生长至关重要。PIF3和HY5在黑暗中拮抗原叶绿素的合成。但是，PIF3 / HY5模块调节参与原叶绿素合成的基因的机制尚不清楚。
• 使用遗传，分子和生化技术，我们发现B‐BOX蛋白BBX11直接作用于PIF3和HY5的下游，以转录调节参与原叶绿素合成的基因。
• 暴露于光线下，深色生长的bbx11和35S：BBX11幼苗的绿化能力分别增强和降低。35S：BBX11幼苗中HEMA1和CHLH的转录水平上调，这些幼苗在黑暗中积累了高水平的原叶绿素内酯，并在光照下发生光漂白。PIF3 通过直接与其启动子结合而在黑暗中抑制 BBX11。bbx11抑制子叶绿化的缺陷 PIF3 延长暗后，表明绿化的PIF3介导的调节是依赖于BBX11。的增强的绿化HY5也被抑制在HY5线过表达BBX11。鉴于此，HY5直接与BBX11的启动子结合并激活其表达以调节BBX11介导的下胚轴抑制作用。
• 我们表明，PIF3 / HY5模块以相反的方式调节BBX11的表达，以优化原叶绿素在黑暗中的积累并促进光的光形态发生。