Dual Role for FHY3 in Light Input to the Clock.

Dual Role for FHY3 in Light Input to the Clock.
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DOI:
10.3389/fpls.2022.862387
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发表时间:
2022
影响因子:
5.6
通讯作者:
--
中科院分区:
生物学2区
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红光调节转录因子FHY3和FAR1在正调控植物生物钟内基因表达中形成了光输入到植物生物钟的关键点。然而,fhy3突变体显示出额外的红光特异性节律性破坏,这与此作用不一致。在这里,我们证明了只有fhy3而不是far1突变体表现出这种红色特异性的节律性破坏。我们研究了节奏转录组在红光和白色光下的差异,揭示了中央时钟蛋白之间节奏模式的差异,这表明时钟的中央机制内的重点变化,这些变化是fhy3突变体的红色特异性的基础。特别是,启动子元件富集的变化与HY5转录因子的关键作用一致,HY5转录因子是一种已知的红蓝光比例调节时钟的整合因子。在红光下检查fhy3突变体中节律性转录组的差异,鉴定了CCA1调节的ELF 3和LUX中央时钟基因的特异性破坏,而CCA1靶TBS元件TGGGCC在变得异常的基因中富集。再加上已知的FHY3,而不是FAR1与CCA1的相互作用,我们提出,红色特定的昼夜节律表型的FHY3可能涉及破坏先前证明的适度的CCA1活动的FHY3,而不是破坏其自身的转录调节活性。总之,这一证据表明,FHY3和HY5之间的条件冗余,在红色和蓝色光输入到时钟的整合,以使可塑性响应光和优化植物适应。此外,我们的证据还表明,红色和白色光转录组之间的CCA 1活性的变化。这与记录的HY5与CCA1的相互作用一起,导致我们提出一种模型,其中红色和蓝色信号的这种整合至少部分地通过FHY3和HY5与CCA1的直接相互作用发生,从而导致CCA1活性的调节。
The red-light regulated transcription factors FHY3 and FAR1 form a key point of light input to the plant circadian clock in positively regulating expression of genes within the central clock. However, the fhy3 mutant shows an additional red light-specific disruption of rhythmicity which is inconsistent with this role. Here we demonstrate that only fhy3 and not far1 mutants show this red specific disruption of rhythmicity. We examined the differences in rhythmic transcriptome in red versus white light and reveal differences in patterns of rhythmicity among the central clock proteins suggestive of a change in emphasis within the central mechanism of the clock, changes which underlie the red specificity of the fhy3 mutant. In particular, changes in enrichment of promoter elements were consistent with a key role for the HY5 transcription factor, a known integrator of the ratio of red to blue light in regulation of the clock. Examination of differences in the rhythmic transcriptome in the fhy3 mutant in red light identified specific disruption of the CCA1-regulated ELF3 and LUX central clock genes, while the CCA1 target TBS element, TGGGCC, was enriched among genes that became arrhythmic. Coupled with the known interaction of FHY3 but not FAR1 with CCA1 we propose that the red-specific circadian phenotype of fhy3 may involve disruption of the previously demonstrated moderation of CCA1 activity by FHY3 rather than a disruption of its own transcriptional regulatory activity. Together, this evidence suggests a conditional redundancy between FHY3 and HY5 in the integration of red and blue light input to the clock in order to enable a plasticity in response to light and optimise plant adaptation. Furthermore, our evidence also suggests changes in CCA1 activity between red and white light transcriptomes. This, together with the documented interaction of HY5 with CCA1, leads us to propose a model whereby this integration of red and blue signals may at least partly occur via direct FHY3 and HY5 interaction with CCA1 leading to moderation of CCA1 activity.
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