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Chilling-responsive strigolactone signaling orchestrates bud break and chilling tolerance in apple.

PubMed · 2026-05-11

Scientists discovered that a plant hormone called strigolactone acts as a molecular switch in apple trees, balancing the competing needs to break winter dormancy and survive prolonged cold. This mechanism explains why apple trees grown in regions with excessively long winters lose the ability to bud out reliably in spring, defining the geographic limits of apple cultivation.

1

Strigolactone hormones serve a dual role in apple trees — suppressing bud break while simultaneously boosting tolerance to prolonged cold stress, with a single protein (D53) acting as the central switch between these two states.

2

During normal chilling, cold temperatures activate transcription factors (CBF4 and TCP14) that build up D53 protein, driving bud break competence; as chilling accumulates further, rising strigolactones accelerate D53 breakdown to prioritize cold survival over dormancy release.

3

Under excessive chilling, elevated strigolactones trigger a phosphorylation cascade that frees the ICE1 protein from D53, activating cold-stress genes at the expense of bud break capacity — a molecular explanation for why orchards in extreme-cold regions show weakened spring flowering.

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