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Circadian and Plastid Signaling Pathways Are Integrated to Ensure Correct Expression of the CBF and COR Genes during Photoperiodic Growth

机译:昼夜节律和质体信号通路集成在一起以确保光周期生长过程中CBF和COR基因的正确表达

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摘要

The circadian clock synchronizes a wide range of biological processes with the dayight cycle, and correct circadian regulation is essential for photosynthetic activity and plant growth. We describe here a mechanism where a plastid signal converges with the circadian clock to fine-tune the regulation of nuclear gene expression in Arabidopsis (Arabidopsis thaliana). Diurnal oscillations of tetrapyrrole levels in the chloroplasts contribute to the regulation of the nucleus-encoded transcription factors C-REPEAT BINDING FACTORS (CBFs). The plastid signal triggered by tetrapyrrole accumulation inhibits the activity of cytosolic HEAT SHOCK PROTEIN90 and, as a consequence, the maturation and stability of the clock component ZEITLUPE (ZTL). ZTL negatively regulates the transcription factor LONG HYPOCOTYL5 (HY5) and PSEUDO-RESPONSE REGULATOR5 (PRR5). Thus, low levels of ZTL result in a HY5- and PRR5-mediated repression of CBF3 and PRR5-mediated repression of CBF1 and CBF2 expression. The plastid signal thereby contributes to the rhythm of CBF expression and the downstream COLD RESPONSIVE expression during dayight cycles. These findings provide insight into how plastid signals converge with, and impact upon, the activity of well-defined clock components involved in circadian regulation.
机译:昼夜节律时钟使各种生物过程与昼/夜周期同步,正确的昼夜节律调节对于光合作用和植物生长至关重要。我们在这里描述一种机制,其中质体信号与昼夜节律时钟会合以微调拟南芥(Arabidopsis thaliana)中核基因表达的调节。叶绿体中四吡咯水平的昼夜振荡有助于调节核编码的转录因子C-重复结合因子(CBF)。由四吡咯积累触发的质体信号抑制了细胞质抗热蛋白90的活性,并因此抑制了时钟组件ZEITLUPE(ZTL)的成熟和稳定性。 ZTL负调控转录因子LONG HYPOCOTYL5(HY5)和PSEUDO-RESPONSE REGULATOR5(PRR5)。因此,低水平的ZTL导致HY5和PRR5介导的CBF3的阻遏和PRR5介导的CBF1和CBF2的表达的阻遏。因此,质体信号有助于昼夜循环中CBF表达的节奏和下游的COLD RESPONSIVE表达。这些发现提供了对质体信号如何与昼夜节律调控中所涉及的明确定义的时钟成分的活动融合并对其产生影响的见解。

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