Abstract

The tradeoff between growth and defense in plants is a core strategy for adaptation, but the mechanisms underlying metabolic flux switching remain incompletely understood. The alpine plant Salix brachista provides an ideal model for studying stress adaptation and metabolic plasticity. Through integrated multi-omics analysis, this study elucidated the transcriptional regulation of phenylpropanoid metabolic flux during the domestication of S. brachista from highland to lowland environments and under chilling stress. Transcriptomic and metabolomic data revealed that plain domestication redirected phenylpropanoid metabolism from the flavonoid branch toward lignin synthesis, reflecting a "defense reduction-growth enhancement" strategy. Conversely, chilling stress reversed this flux by downregulation of lignin biosynthesis genes (COMT, F5H, CAD, CCR) and upregulation of flavonoid biosynthesis genes (PAL, CHS, CHI). We identified two chilling-responsive transcription factors, SbrMYB113 and SbrWRKY51, which formed a co-expression module with PAL, 4CL, CHS, and CHI (r > 0.8). DNA affinity purification sequencing (DAP-seq) confirmed significant enrichment of the SbrWRKY51 binding motif (AAAAAGTCAAMVH) in the promoter regions of phenylpropanoid genes. Dual-luciferase (LUC) assays demonstrated that SbrMYB113 significantly transactivates the SbrPAL1 and SbrPAL4 promoters. This regulatory function was further validated by the heterologous expression of SbrMYB113 in Arabidopsis thaliana. Cross-species analysis revealed that this regulatory module is evolutionarily conserved. In conclusion, S. brachista regulates phenylpropanoid flux via a chilling-responsive module involving SbrMYB113/SbrWRKY51 and downstream genes (SbrPAL, Sbr4CL, SbrCHS, SbrCHI), enabling reversible growth-defense tradeoffs.