Zhao Jing, Li Juzuo, Lei Xiujuan, Di Peng, Xun Hongwei, Zhang Zhibin, Zhang Jian, Meng Xiangru, Wang Yingping
College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
State Local Joint Engineering Research Centre of Ginseng Breeding and Application, Jilin Agricultural University, Changchun 130118, China.
Plants (Basel). 2025 Jul 9;14(14):2120. doi: 10.3390/plants14142120.
Ginseng rusty root symptoms (GRSs) compromise the yield and quality of . While transcriptomic analyses have demonstrated extensive remodeling of stress signaling networks, the post-transcriptional defense circuitry remains obscure. We profiled alternative splicing (AS) in three phloem tissues, the healthy phloem (AG), the non-reddened phloem neighboring lesions (BG), and the reddened lesion core (CG), to delineate AS reprogramming during GRS progression. The frequency of AS was sharply elevated in CG, with intron retention predominating. Extensive gains and losses of splice events indicate large-scale rewiring of the splice network. Overlapping differentially alternative spliced genes (DAGs) identified in both CG vs AG and CG vs BG contrasts were significantly enriched for RNA-spliceosome assembly and stress-response pathways, revealing a conserved post-transcriptional response associated with lesion formation. Integrative analysis of differentially expressed genes uncovered 671 loci under dual regulation; functional classification categorized these genes in receptor-like kinase signaling and chromatin-remodeling modules, underscoring the synergy between AS and transcriptional control. Moreover, the B subgenome disproportionately contributed stress-responsive transcripts in diseased tissue, suggesting an adaptive, subgenome-biased strategy. These findings demonstrate that dynamic AS remodeling and subgenome expression bias jointly orchestrate ginseng defense against GRS and provide a framework for breeding disease-resilient crops.
人参锈根症状（GRSs）会影响人参的产量和品质。虽然转录组分析已经证明了应激信号网络的广泛重塑，但转录后防御机制仍不清楚。我们对三种韧皮部组织中的可变剪接（AS）进行了分析，即健康韧皮部（AG）、邻近病变的未变红韧皮部（BG）和变红的病变核心（CG），以描绘GRS进展过程中的AS重编程。CG中的AS频率急剧升高，内含子保留占主导。剪接事件的大量增减表明剪接网络的大规模重新布线。在CG与AG和CG与BG对比中鉴定出的重叠差异可变剪接基因（DAGs）在RNA剪接体组装和应激反应途径中显著富集，揭示了与病变形成相关的保守转录后反应。对差异表达基因的综合分析发现了671个受双重调控的基因座；功能分类将这些基因归类于类受体激酶信号传导和染色质重塑模块，强调了AS与转录控制之间的协同作用。此外，B亚基因组在患病组织中对应激反应转录本的贡献不成比例，表明存在一种适应性的、亚基因组偏向的策略。这些发现表明，动态AS重塑和亚基因组表达偏向共同协调人参对GRS的防御，并为培育抗病作物提供了一个框架。
