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PtoHY5 integrates photoperiodic signals with the ABA pathway to coordinate growth cessation and dormancy in Populus

Hongbin Wei1,2†*, Junlong Shen1†, Yongfeng Gao3†, Yue Xiao1, Fan Sun1, Miao Fang1, Qin Song1, Xiang Liu1, Yinan Yao3 and Keming Luo1,2*   

  1. 1. Chongqing Key Laboratory of Forest Resource Innovation and Utilization, Integrative Science Center of Germplasm Creation in Western China (Chongqing) Science City, School of Life Sciences, Southwest University, Chongqing 400715, China
    2. Key Laboratory of Eco‐environments of Three Gorges Reservoir Region, Ministry of Education, School of Life Sciences, Southwest University, Chongqing 400715, China
    3. School of Life Science and Engineering, Southwest University of Science and Technology, Mianyang 621010, China

    †These authors contributed equally to this work.
    *Correspondences: Keming Luo (kemingl@swu.edu.cn, Dr. Luo is fully responsible for the distribution of all materials associated with this article); Hongbin Wei (hongbinwei@swu.edu.cn)
  • Received:2026-02-23 Accepted:2026-06-24 Online:2026-07-16
  • Supported by:
    This work was supported by the National Natural Science Foundation of China (32572011, 32371903), New Chongqing Youth Innovation Talent Program (2025YITP‐QCRCX0311), Biological Breeding‐National Science and Technology Major Project (2023ZD04068), Fundamental Research Funds for the Central Universities (SWU‐KT26039), and Southwest University Graduate Research and Innovation Project (SWUB25042).

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Abstract: Perennial plants in boreal and temperate climates synchronize their growth-dormancy cycles with seasonal changes. At the same time, short-day (SD) conditions are known to induce growth cessation through downregulation of the growth-promoting gene FLOWERING LOCUS T2 (FT2) and promote dormancy establishment via an abscisic acid (ABA)-dependent pathway. Yet how photoperiodic signals coordinate these transitions remains unclear; in particular, the role of ABA in SD-induced growth cessation is underappreciated. Here, we demonstrate that ABA-deficient nced1/3 mutants display delayed growth arrest and impaired dormancy, indicating that ABA coordinates SD-triggered growth cessation with dormancy establishment. We identify the Populus ELONGATED HYPOCOTYL 5 (PtoHY5a/b) transcription factors as central integrators of long-day signals that maintain active growth. Overexpression of PtoHY5a/b delays growth cessation and impedes dormancy establishment by suppressing plasmodesmata closure in shoot apices; these effects are reversed by exogenous ABA application. Mechanistically, PtoHY5 directly represses ABA biosynthesis genes PtoNCED1/3 and the dormancy-promoting gene SHORT VEGETATIVE PHASE-LIKE (PtoSVL). Furthermore, PtoHY5 acts locally in leaves and shoot apices and moves from leaves to the apex to fine-tune apical growth. Under SD conditions, decreased PtoHY5 levels lead to coordinated downregulation of PtoFT2 (the accelerator) and activation of the ABA-PtoSVL axis (the brake), thereby synchronizing growth cessation and dormancy initiation. These findings clarify the disputed role of ABA in growth cessation and uncover a previously unknown regulatory layer centered on PtoHY5 that integrates photoperiodic signals with the coordination of growth cessation and dormancy initiation in perennial trees.

Key words: ABA, dormancy initiation, growth cessation, mobile HY5, photoperiod perception, Populus

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