The seasonal growth-dormancy cycle constitutes a fundamental survival strategy for perennial woody plants in temperate ecosystems. While this developmental plasticity is orchestrated by environmental cues, it exhibits profound age-dependent modulation. The molecular circuitry governing dormancy is well-charted in short-lived angiosperm models. However, the mechanisms by which ancient, long-lived conifers dynamically adjust their environmental responsiveness across centuries of ontogeny remain elusive. Here, using Pinus tabuliformis as a model, we integrated transcriptomics, weighted gene co-expression network analysis (WGCNA), and biochemical assays to dissect the pathway integrating age signals into the dormancy network. We found that the MADS-box age-marker PtDAL1 is significantly upregulated in dormant buds of 3-year-old saplings compared to juvenile seedlings. Although PtDAL1 transcriptionally activates the dormancy-marker PtTFL2, endogenous profiling revealed a strict inverse correlation, with PtTFL2 expression declining as trees mature. Mechanistically, we demonstrate that PtDAL1 not only binds the PtTFL2 promoter but also physically recruits the SVP-like protein PtDAL21 to sequester PtTFL2 into a stable complex. We propose that this complex formation overrides transcriptional dynamics, thereby elevating the threshold for dormancy release. This mechanism underpins the deep dormancy and phenological recalcitrance observed in adult trees, ensuring survival against premature spring awakening. Our findings bridge a critical gap in gymnosperm ontogeny and provide molecular targets for adapting forest phenology to global climate change.
Keywords: Age-dependent modulation; DAL1; Dormancy; Mads-box; Pinus tabuliformis; TFL2.
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