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<p>Poplar is a key tree species in temperate and subtropical regions, particularly valued in China for its rapid growth and versatility in forestry. Among various cultivars, Poplar 107 is recognized for its superior qualities, including drought and pest resistance. However, diseases like gray spot disease, caused by <i>C. populinum</i>, threaten poplar productivity. Current reliance on chemical pesticides is problematic due to potential resistance and environmental concerns, highlighting the need for disease-resistant cultivars. This study investigates the molecular mechanisms behind poplar’s response, focusing on secondary metabolite-mediated resistance. Transcriptomic and metabolomic analyses revealed significant upregulation of flavonoid biosynthesis pathways post-infection, accompanied by accumulation of key antimicrobial compounds (e.g., naringenin and catechin). Functional enrichment analysis identified 34 differentially expressed genes (DEGs) in the flavonoid pathway, including phenylalanine ammonia-lyase (<i>FLS</i>), chalcone synthase (<i>CHS</i>), and flavonol synthase (<i>PAL</i>). Transcription factors from the MYB and WRKY families exhibited strong positive correlations with phenylpropanoid biosynthesis gene expression networks. Metabolomic profiling confirmed 273 differentially abundant metabolites (DAMs), with flavonoid derivatives dominating the upregulated profile. Integrated multi-omics analysis demonstrated that <i>C. populinum</i> infection triggers a systemic defense response characterized by: (i) activation of phenylpropanoid/flavonoid biosynthesis pathways; (ii) accumulation of antimicrobial flavonoids; (iii) modulation of antioxidative enzyme activities; and (iv) transcriptional reprogramming involving MYB/WRKY-mediated regulatory networks. These findings advance our mechanistic understanding of poplar–fungus interactions and provide actionable insights for developing sustainable disease management strategies through metabolic engineering and marker-assisted breeding.</p>

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Enhanced flavonoid levels as a key response to Coryneum populinum infection in Populus × euramericana cv. ‘74/76’ (Poplar 107): insights from transcriptomic and metabolomic analyses

  • 期刊论文

  • 发表日期：

    2025年4月21日

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  • Jun Feng,
  • Huan Liu,
  • Wanzhuang Ma,
  • Yu Xiu,
  • Huilong Zhang,
  • Xiuli Tang

摘要

Poplar is a key tree species in temperate and subtropical regions, particularly valued in China for its rapid growth and versatility in forestry. Among various cultivars, Poplar 107 is recognized for its superior qualities, including drought and pest resistance. However, diseases like gray spot disease, caused by C. populinum, threaten poplar productivity. Current reliance on chemical pesticides is problematic due to potential resistance and environmental concerns, highlighting the need for disease-resistant cultivars. This study investigates the molecular mechanisms behind poplar’s response, focusing on secondary metabolite-mediated resistance. Transcriptomic and metabolomic analyses revealed significant upregulation of flavonoid biosynthesis pathways post-infection, accompanied by accumulation of key antimicrobial compounds (e.g., naringenin and catechin). Functional enrichment analysis identified 34 differentially expressed genes (DEGs) in the flavonoid pathway, including phenylalanine ammonia-lyase (FLS), chalcone synthase (CHS), and flavonol synthase (PAL). Transcription factors from the MYB and WRKY families exhibited strong positive correlations with phenylpropanoid biosynthesis gene expression networks. Metabolomic profiling confirmed 273 differentially abundant metabolites (DAMs), with flavonoid derivatives dominating the upregulated profile. Integrated multi-omics analysis demonstrated that C. populinum infection triggers a systemic defense response characterized by: (i) activation of phenylpropanoid/flavonoid biosynthesis pathways; (ii) accumulation of antimicrobial flavonoids; (iii) modulation of antioxidative enzyme activities; and (iv) transcriptional reprogramming involving MYB/WRKY-mediated regulatory networks. These findings advance our mechanistic understanding of poplar–fungus interactions and provide actionable insights for developing sustainable disease management strategies through metabolic engineering and marker-assisted breeding.