English
Cytospora chrysosperma induces severe canker disease in poplars, causing substantial economic and ecological losses. The mechanisms underlying poplar resistance to this pathogen remain poorly understood. This study evaluates resistance in three poplar species, identifying Populus × canadensis and Populus × beijingensis as resistant, and Populus tomentosa as susceptible. Multi-omics analyses revealed that resistant poplars upregulate defense-related genes, particularly those involved in lignin biosynthesis and hormone signaling. Integrated transcript-metabolite networks demonstrated coordinated activation of phenylpropanoid pathway genes (e.g., PAL, 4CL, CAD) and accumulation of antifungal metabolites in resistant species. Key metabolites, including ferulic acid, p-coumaraldehyde, and cinnamic acid, exhibited strong antifungal activity, completely inhibiting C. chrysosperma growth. Transcriptomic data further confirmed enhanced expression of genes associated with lignin biosynthesis and cell wall reinforcement in resistant poplars. The phenylpropanoid pathway is central to poplar resistance, orchestrating metabolic and structural defenses. These insights provide a foundation for breeding programs aimed at enhancing resistance and offer strategies for forestry management to mitigate fungal disease impacts.