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拟南芥转录因子TCP5通过正向调控PIF4活性来控制植物的热形态建成。

Arabidopsis Transcription Factor TCP5 Controls Plant Thermomorphogenesis by Positively Regulating PIF4 Activity.

作者信息

Han Xiang, Yu Hao, Yuan Rongrong, Yang Yan, An Fengying, Qin Genji

机构信息

State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing 100871, The People's Republic of China; The Peking-Tsinghua Center for Life Sciences, Beijing 100871, The People's Republic of China; Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, The People's Republic of China.

State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing 100871, The People's Republic of China.

出版信息

iScience. 2019 May 31;15:611-622. doi: 10.1016/j.isci.2019.04.005. Epub 2019 May 8.

Abstract

Plants display thermomorphogenesis in response to high temperature (HT). PHYTOCHROME INTERACTING FACTOR 4 (PIF4) is a central integrator regulated by numerous negative regulators. However, the mechanisms underpinning PIF4 positive regulation are largely unknown. Here, we find that TEOSINTE BRANCHED 1/CYCLOIDEA/PCF 5 (TCP5), TCP13, and TCP17 transcription factors promote the activity of PIF4 at transcriptional and post-transcriptional levels. TCP5 is rapidly induced by HT treatment, and TCP5 protein stability increases under HT. The overexpression of TCP5 causes constitutive thermomorphogenic phenotypes, whereas the tcp5 tcp13 tcp17 triple mutant exhibits aberrant thermomorphogenesis. We demonstrate that TCP5 not only physically interacts with PIF4 to enhance its activity but also directly binds to the promoter of PIF4 to increase its transcript. TCP5 and PIF4 share common downstream targets. The tcp5 tcp13 tcp17 mutant partially restores the long hypocotyls caused by PIF4 overexpression. Our findings provide a layer of understanding about the fine-scale regulation of PIF4 and plant thermomorphogenesis.

摘要

植物在高温(HT)响应中表现出热形态建成。光敏色素相互作用因子4(PIF4)是一个受众多负调控因子调节的核心整合因子。然而,PIF4正调控的机制在很大程度上尚不清楚。在这里,我们发现玉米分枝1/环化酶/PCF 5(TCP5)、TCP13和TCP17转录因子在转录和转录后水平上促进PIF4的活性。HT处理可快速诱导TCP5,且HT条件下TCP5蛋白稳定性增加。过表达TCP5会导致组成型热形态建成表型,而tcp5 tcp13 tcp17三突变体则表现出异常的热形态建成。我们证明,TCP5不仅与PIF4发生物理相互作用以增强其活性,还直接结合到PIF4的启动子上以增加其转录本。TCP5和PIF4共享共同的下游靶标。tcp5 tcp13 tcp17突变体部分恢复了由PIF4过表达导致的长下胚轴。我们的研究结果为PIF4和植物热形态建成的精细调控提供了一层理解。

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