Arabidopsis clock-associated pseudo-response regulators PRR9, PRR7 and PRR5 coordinately and positively regulate flowering time through the canonical CONSTANS-dependent photoperiodic pathway
Arabidopsis clock-associated pseudo-response regulators PRR9, PRR7 and PRR5 coordinately and positively regulate flowering time through the canonical CONSTANS-dependent photoperiodic pathway
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DOI：
10.1093/pcp/pcm056
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发表时间：
2007-06-01
影响因子：
4.9
通讯作者：
Mizuno, Takeshi
中科院分区：
文献类型：
--
作者：
Nakamichi, Norihito;Kita, Masanori;Mizuno, Takeshi
光周期使生物能够测量日长或外部光周期，并预测即将到来的季节。昼长测量需要通过生物钟将光信号和时间信息结合起来。在长日照植物拟南芥中，CONSTANS（CO）在将昼夜节律和环境光信号整合到光周期开花途径中起着至关重要的作用。然而，生物钟调节CO循环表达谱的分子机制知之甚少。在这里，我们首先表明，时钟相关基因伪反应调节因子（PRR）PRR 9，PRR 7和PRR 5参与白天CO表达的激活。然后，使用昼夜节律钟相关1（CCA 1）/晚伸长下胚轴（LHY）双突变体（cca 1/lhy）和prr 7/prr 5进行了广泛的遗传研究。结果表明，PRR基因与CCA/LHY在典型的CO-FLOW LOCUS T（FT）光周期开花途径的上游以平行和拮抗的方式协同作用。最后，我们提供的证据提出了一个模型，其中CCA 1/LHY通过GIGANTEA（GI）抑制CO，而PRR 9，PRR 7和PRR 5主要通过抑制编码DNA结合转录抑制因子的循环自由度因子1（CDF 1）激活CO。
Photoperiodism allows organisms to measure daylength, or external photoperiod, and to anticipate coming seasons. Daylength measurement requires the integration of light signal and temporal information by the circadian clock. In the long-day plant Arabidopsis thaliana, CONSTANS (CO) plays a crucial role in integrating the circadian rhythm and environmental light signals into the photoperiodic flowering pathway. Nevertheless, the molecular mechanism by which the circadian clock modulates the cyclic expression profile of CO is poorly understood. Here, we first showed that the clock-associated genes PSEUDO-RESPONSE REGULATOR (PRR) PRR9, PRR 7 and PRR5 are involved in activation of CO expression during the daytime. Then, extensive genetic studies using CIRCADIAN CLOCK-ASSOCIATED1 (CCA1)/LATE ELONGATED HYPOCOTYL (LHY) double mutants (cca1/lhy) and prr7/ prr5 were conducted. The results suggested that PRR genes act coordinately in a manner parallel with and antagonistic to CCA/LHY, upstream of the canonical CO-FLOWERING LOCUS T (FT) photoperiodic flowering pathway. Finally, we provided evidence to propose a model, in which CCA1/LHY repress CO through GIGANTEA (GI), while PRR9, PRR7 and PRR5 activate CO predominantly by repressing CYCLING DOF FACTOR1 (CDF1) encoding a DNA-binding transcriptional repressor.