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<p>Anthracnose disease, caused by <i>Colletotrichum</i> species, poses a significant threat to global litchi production, yet the molecular mechanisms governing host resistance remain poorly understood. To dissect the genetic basis of anthracnose resistance, we employed a comparative transcriptomic approach using two contrasting cultivars: ‘YuJinQiu’ (DR, disease-resistant genotype) and ‘BaiTangYing’ (DS, disease-susceptible genotype). Field evaluations and controlled infection assays demonstrated evident phenotypic divergence, with DR exhibiting delayed disease progression and 43.7% smaller lesion areas compared to DS at 72&#xa0;h post-inoculation (hpi). Time-resolved RNA sequencing (0–72 hpi) revealed genotype-specific transcriptional dynamics, where DR displayed fewer differentially expressed genes (DEGs; 819–1457) compared to DS (5195–5735), suggesting a more targeted and efficient defense response. Functional enrichment analyses highlighted rapid activation of innate immunity pathways in DR, including pattern-triggered immunity, MAPK signaling, and jasmonic acid/ethylene biosynthesis, whereas DS prioritized cell wall modification and compensatory secondary metabolic processes. Weighted gene co-expression network analysis (WGCNA) pinpointed three modules tightly linked to anthracnose resistance, enriched for receptor-like kinases (RLKs), nucleotide-binding leucine-rich repeat (NLR) proteins, and phenylpropanoid biosynthesis genes. Hub regulators, including WRKY transcription factors (e.g., WRKY33), ubiquitin ligases, and pathogenesis-related proteins (PR1, PR5), were identified as central coordinators of defense signaling. Strikingly, DR exhibited sustained upregulation of effector-triggered immunity markers, particularly nucleotide-binding leucine-rich repeat (NLR) genes, and early accumulation of phytoalexins, correlating with pathogen suppression. Experimental validation via qRT-PCR confirmed the reliability of transcriptomic data. Our study unravels the multilayer regulatory network underlying litchi anthracnose resistance, providing not only a mechanistic model of cultivar-specific responses but also a robust gene toolkit for accelerating the development of resistant cultivars through marker-assisted breeding.</p>

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Comparative transcriptome analysis unravels genotype-specific defense strategies in anthracnose-resistant and susceptible litchi cultivars

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月11日

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  • Zhaowei Xu,
  • Jiefeng Liu,
  • Junsheng Zhao,
  • Sha Li,
  • Lejun Ouyang,
  • Chao Shen,
  • Ling Zhang,
  • Yongguo Zhao,
  • Junxia Wang,
  • Guangyuan Lu

摘要

Anthracnose disease, caused by Colletotrichum species, poses a significant threat to global litchi production, yet the molecular mechanisms governing host resistance remain poorly understood. To dissect the genetic basis of anthracnose resistance, we employed a comparative transcriptomic approach using two contrasting cultivars: ‘YuJinQiu’ (DR, disease-resistant genotype) and ‘BaiTangYing’ (DS, disease-susceptible genotype). Field evaluations and controlled infection assays demonstrated evident phenotypic divergence, with DR exhibiting delayed disease progression and 43.7% smaller lesion areas compared to DS at 72 h post-inoculation (hpi). Time-resolved RNA sequencing (0–72 hpi) revealed genotype-specific transcriptional dynamics, where DR displayed fewer differentially expressed genes (DEGs; 819–1457) compared to DS (5195–5735), suggesting a more targeted and efficient defense response. Functional enrichment analyses highlighted rapid activation of innate immunity pathways in DR, including pattern-triggered immunity, MAPK signaling, and jasmonic acid/ethylene biosynthesis, whereas DS prioritized cell wall modification and compensatory secondary metabolic processes. Weighted gene co-expression network analysis (WGCNA) pinpointed three modules tightly linked to anthracnose resistance, enriched for receptor-like kinases (RLKs), nucleotide-binding leucine-rich repeat (NLR) proteins, and phenylpropanoid biosynthesis genes. Hub regulators, including WRKY transcription factors (e.g., WRKY33), ubiquitin ligases, and pathogenesis-related proteins (PR1, PR5), were identified as central coordinators of defense signaling. Strikingly, DR exhibited sustained upregulation of effector-triggered immunity markers, particularly nucleotide-binding leucine-rich repeat (NLR) genes, and early accumulation of phytoalexins, correlating with pathogen suppression. Experimental validation via qRT-PCR confirmed the reliability of transcriptomic data. Our study unravels the multilayer regulatory network underlying litchi anthracnose resistance, providing not only a mechanistic model of cultivar-specific responses but also a robust gene toolkit for accelerating the development of resistant cultivars through marker-assisted breeding.