In response to competition for light from their neighbors, shade-intolerant plants flower precociously to ensure reproductive success and survival. However, the molecular mechanisms underlying this key developmental switch are not well understood. Here, we show that a pair of Arabidopsis transcription factors essential for phytochrome A signaling, FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and FAR-RED IMPAIRED RESPONSE1 (FAR1), regulate flowering time by integrating environmental light signals with the miR156-SPL module-mediated aging pathway. We found that FHY3 and FAR1 directly interact with three flowering-promoting SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors, SPL3, SPL4, and SPL5, and inhibit their binding to the promoters of several key flowering regulatory genes, including FRUITFUL (FUL), LEAFY (LFY), APETALA1 (AP1), and MIR172C, thus downregulating their transcript levels and delaying flowering. Under simulated shade conditions, levels of SPL3/4/5 proteins increase, whereas levels of FHY3 and FAR1 proteins decline, thus releasing SPL3/4/5 from FHY3/FAR1 inhibition to allow activation of FUL, LFY, AP1, and MIR172C and, consequently, early flowering. Taken together, these results unravel a novel mechanism whereby plants regulate flowering time by integrating environmental cues (such as light conditions) and an internal developmental program (the miR156-SPL module-mediated aging pathway).

为了抵抗邻居的争光，不耐荫的植物早熟开花，以确保繁殖成功和生存。但是，这种关键的发展转换背后的分子机制还不是很清楚。在这里，我们显示了对植物色素A信号必不可少的拟南芥转录因子，FAR-RED加长HYPOCOTYL3（FHY3）和FAR-RED受损反应1（FAR1），它们通过将环境光信号与miR156-SPL模块-整合在一起来调节开花时间。介导的衰老途径。我们发现FHY3和FAR1直接与三个促进开花的SQUAMOSA-PROMOTER BINDING蛋白类似（SPL）转录因子，SPL3，SPL4和SPL5相互作用，并抑制它们与几个关键开花调节基因的启动子结合，包括硕果累累（FUL），LEAFY（LFY），APETALA1（AP1），并MIR172C，因而下调其转录水平和延迟开花。在模拟的阴影条件下，SPL3 / 4/5蛋白的水平增加，而FHY3和FAR1蛋白的水平下降，因此从FHY3 / FAR1抑制中释放SPL3 / 4/5，以激活FUL，LFY，AP1和MIR172C 因此，早开花。综上所述，这些结果揭示了一种新颖的机制，该植物通过整合环境线索（例如光照条件）和内部发育程序（miR156-SPL模块介导的衰老途径）来调节开花时间。