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

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.