The circadian clock measures and conveys daylength information to control rhythmic hypocotyl growth in photoperiodic conditions to achieve optimal fitness, but it operates through largely unknown mechanisms. Here, we show that Pseudo Response Regulators (PRRs) coordinate with the Evening Complex (EC), a transcriptional repressor complex within the clock core oscillator, to specifically regulate photoperiodic hypocotyl growth in Arabidopsis (Arabidopsis thaliana). Intriguingly, a distinct daylength could shift the expression phase and extend the expression duration of PRRs. Multiple lines of evidence have further demonstrated that PRRs directly bind the promoters of PHYTOCHROME-INTERACTING FACTOR4 (PIF4) and PIF5 to repress their expression, hence PRRs act as transcriptional repressors of the positive growth regulators PIF4 and PIF5. Importantly, mutation or truncation of the TIMING OF CAB EXPRESSION1 (TOC1) DNA binding domain, without compromising its physical interaction with PIFs, still caused long hypocotyl growth under short days, highlighting the essential role of the PRR-PIF transcriptional module in photoperiodic hypocotyl growth. Finally, genetic analyses have demonstrated that PIF4 and PIF5 are epistatic to PRRs in the regulation of photoperiodic hypocotyl growth. Collectively, we propose that, upon perceiving daylength information, PRRs cooperate with EC to directly repress PIF4 and PIF5 transcription together with their posttranslational regulation of PIF activities, thus forming a complex regulatory network to mediate circadian clock-regulated photoperiodic growth.

昼夜节律时钟可以测量并传达日长信息，以控制光周期条件下节律性下胚轴的生长，以达到最佳适应性，但它​​的运行机制很大程度上未知。在这里，我们显示伪响应调节器（PRRs）与时钟复合体中的转录阻遏物复合体-晚复合物（EC）协调，以专门调节拟南芥（Arabidopsis thaliana）的光周期下胚轴生长。有趣的是，不同的日长可能会改变表达相位并延长PRR的表达持续时间。多种证据进一步表明，PRR直接结合PHYTOCHROME-INTERACTING FACTOR4（PIF4）和PIF5的启动子抑制其表达，因此PRR充当正向生长调节因子PIF4和PIF5的转录抑制因子。重要的是，在不损害CAB EXPRESSION1（TOC1）DNA结合结构域与PIF物理相互作用的情况下，突变或截短仍会导致短胚轴长时间生长，这突出了PRR -PIF转录模块在光周期下胚轴生长中的重要作用。。最后，遗传分析表明，PIF4和PIF5在光周期下胚轴生长的调节中对PRR具有上位性。总体而言，我们建议，在了解日长信息后，PRR与EC合作直接抑制PIF4和PIF5转录以及它们对PIF活性的翻译后调节，从而形成一个复杂的调节网络来介导昼夜节律调节的光周期生长。