J Integr Plant Biol ›› 2024, Vol. 66 ›› Issue (1): 20-35.DOI: 10.1111/jipb.13579

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  • 收稿日期:2023-06-26 接受日期:2023-10-25 出版日期:2024-01-01 发布日期:2024-01-25

Heat Shock Factor A1s are required for phytochrome-interacting factor 4-mediated thermomorphogenesis in Arabidopsis

Bingjie Li1†, Shimeng Jiang1†, Liang Gao1†, Wenhui Wang1, Haozheng Luo1, Yining Dong1, Zhihua Gao2, Shuzhi Zheng1, Xinye Liu1* and Wenqiang Tang1*   

  1. 1. Key Laboratory of Molecular and Cellular Biology of Ministry of Education, Hebei Research Center of the Basic Discipline of Cell Biology; Hebei Collaboration Innovation Center for Cell Signaling, Hebei Key Laboratory of Molecular and Cellular Biology, College of Life Sciences, Hebei Normal University, Shijiazhuang 050024, China;
    2. School of Information Technology, Hebei University of Economics and Business, Shijiazhuang 050061, China
    †These authors contributed equally to this work.
    *Correspondences: Xinye Liu (xinyeliu@hebtu.edu.cn); Wenqiang Tang (tangwq@hebtu.edu.cn, Dr. Tang is fully responsible for the distribution of all materials associated with this article)
  • Received:2023-06-26 Accepted:2023-10-25 Online:2024-01-01 Published:2024-01-25

Abstract: Thermomorphogenesis and the heat shock (HS) response are distinct thermal responses in plants that are regulated by PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) and HEAT SHOCK FACTOR A1s (HSFA1s), respectively. Little is known about whether these responses are interconnected and whether they are activated by similar mechanisms. An analysis of transcriptome dynamics in response to warm temperature (28℃) treatment revealed that 30 min of exposure activated the expression of a subset of HSFA1 target genes in Arabidopsis thaliana. Meanwhile, a loss-of-function HSFA1 quadruple mutant (hsfa1-cq) was insensitive to warm temperature-induced hypocotyl growth. In hsfa1-cq plants grown at 28℃, the protein and transcript levels of PIF4 were greatly reduced, and the circadian rhythm of many thermomorphogenesis-related genes (including PIF4) was disturbed. Additionally, the nuclear localization of HSFA1s and the binding of HSFA1d to the PIF4 promoter increased following warm temperature exposure, whereas PIF4 overexpression in hsfa1-cq partially rescued the altered warm temperature-induced hypocotyl growth of the mutant. Taken together, these results suggest that HSFA1s are required for PIF4 accumulation at a warm temperature, and they establish a central role for HSFA1s in regulating both thermomorphogenesis and HS responses in Arabidopsis.

Key words: HSFA1, PIF4, thermomorphogenesis

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