J Integr Plant Biol ›› 2020, Vol. 62 ›› Issue (11): 1717-1740.DOI: 10.1111/jipb.12971

所属专题: Light signaling

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  • 收稿日期:2020-03-08 接受日期:2020-05-18 出版日期:2020-11-01 发布日期:2020-05-18

FKF1 F-box protein promotes flowering in part by negatively regulating DELLA protein stability under long-day photoperiod in Arabidopsis

Jindong Yan1,2†, Xinmei Li1,2†, Bingjie Zeng1,2, Ming Zhong1,2, Jiaxin Yang1,2, Piao Yang1,2, Xin Li1,2, Chongsheng He1, Jianzhong Lin1, Xuanming Liu1* and Xiaoying Zhao1,2*   

  1. 1College of Biology, Hunan Province Key Laboratory of Plant Functional Genomics and Developmental Regulation, State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China
    2Shenzhen Institute, Hunan University, Shenzhen, 518057, China

    *Correspondences:
    Email: Xuanming Liu (xmL05@hnu.edu.cn); Xiaoying Zhao (xiaoyzhao@hnu.edu.cn, Dr. Zhao is fully responsible for the distribution of all materials associated this article)
  • Received:2020-03-08 Accepted:2020-05-18 Online:2020-11-01 Published:2020-05-18

Abstract:

FLAVIN‐BINDING KELCH REPEAT F‐BOX 1 (FKF1) encodes an F‐box protein that regulates photoperiod flowering in Arabidopsis under long‐day conditions (LDs). Gibberellin (GA) is also important for regulating flowering under LDs. However, how FKF1 and the GA pathway work in concert in regulating flowering is not fully understood. Here, we showed that the mutation of FKF1 could cause accumulation of DELLA proteins, which are crucial repressors in GA signaling pathway, thereby reducing plant sensitivity to GA in flowering. Both in vitro and in vivo biochemical analyses demonstrated that FKF1 directly interacted with DELLA proteins. Furthermore, we showed that FKF1 promoted ubiquitination and degradation of DELLA proteins. Analysis of genetic data revealed that FKF1 acted partially through DELLAs to regulate flowering under LDs. In addition, DELLAs exerted a negative feedback on FKF1 expression. Collectively, these findings demonstrate that FKF1 promotes flowering partially by negatively regulating DELLA protein stability under LDs, and suggesting a potential mechanism linking the FKF1 to the GA signaling DELLA proteins.

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