ArticleScientific reports2026
Comparative transcriptome analysis unravels genotype-specific defense strategies in anthracnose-resistant and susceptible litchi cultivars.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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