MdBRC1 and MdFT2 Interaction Fine-Tunes Bud Break Regulation in Apple

Winter bud dormancy is a critical adaptive process in temperate fruit trees, safeguarding meristems from freezing temperatures and aligning growth with seasonal cues. Dormancy encompasses two primary phases: endodormancy, where internal signals, particularly elevated abscisic acid (ABA), block growth and necessitate chilling for release; and ecodormancy, where buds regain growth competence but remain quiescent until external conditions are favourable. In apple (Malus domestica), we demonstrated that BRANCHED1 (MdBRC1) serves as a central inhibitor of bud growth specifically during ecodormancy. In many plant species, BRC1-like transcription factors integrate environmental and hormonal signals, activating gene networks linked to growth repression, notably those involved in ABA biosynthesis and signalling. Gain-of-function studies in poplar confirmed that MdBRC1 robustly suppresses shoot growth in trees. Our comparative transcriptomic analyses revealed that MdBRC1 directly regulates a suite of dormancy-associated genes, reinforcing its role as a molecular brake on bud break. Importantly, we show that the apple gene FLOWERING LOCUS T2 (MdFT2) is transcriptionally upregulated after dormancy and might act as a key inducer of bud break. Our data reveal that MdFT2 physically interacts with MdBRC1, reducing MdBRC1 activity during ecodormancy. This antagonistic interaction acts as a molecular switch, facilitating the transition from ecodormancy to active bud growth as spring approaches. Together, these findings uncover a regulatory module that finely tunes bud break timing in apple trees and provide a foundation for breeding strategies to enhance fruit tree resilience and adaptability in the context of climate change.