Chen Xiaohong, Fang Fang, Chen Tingting, Wu Jinghua, Zheng Zheng, Deng Xiaoling
Guangdong Province Key Laboratory of Microbial Signals and Disease Control, South China Agricultural University, Guangzhou 510642, China.
Int J Mol Sci. 2025 Jul 30;26(15):7359. doi: 10.3390/ijms26157359.
Huanglongbing (HLB), caused by Liberibacter asiaticus (CLas), is the most devastating disease threatening global citrus production. Although no commercial citrus varieties exhibit complete HLB resistance, genotype-specific tolerance variations remain underexplored. This study conducted a comparative transcriptomic profiling of six commercially citrus cultivars in South China, four susceptible cultivars ( cv. Tankan, Gongkan, Shatangju, and Osbeck cv. Newhall), and two tolerant cultivars ( cv. Eureka; cv Guanxi Yu) to dissect molecular mechanisms underlying HLB responses. Comparative transcriptomic analyses revealed extensive transcriptional reprogramming, with tolerant cultivars exhibiting fewer differentially expressed genes (DEGs) and targeted defense activation compared to susceptible genotypes. The key findings highlighted the genotype-specific regulation of starch metabolism, where β-amylase 3 () was uniquely upregulated in tolerant varieties, potentially mitigating starch accumulation. Immune signaling diverged significantly: tolerant cultivars activated pattern-triggered immunity (PTI) via receptor-like kinases () and suppressed ROS-associated RBOH genes, while susceptible genotypes showed the hyperactivation of ethylene signaling and oxidative stress pathways. Cell wall remodeling in susceptible cultivars involved upregulated xyloglucan endotransglucosylases (), contrasting with pectin methylesterase induction in tolerant Eureka lemon for structural reinforcement. Phytohormonal dynamics revealed SA-mediated defense and NPR3/4 suppression in Eureka lemon, whereas susceptible cultivars prioritized ethylene/JA pathways. These findings delineate genotype-specific strategies in citrus-CLas interactions, identifying , , and cell wall modifiers as critical targets for breeding HLB-resistant cultivars through molecular-assisted selection. This study provides a foundational framework for understanding host-pathogen dynamics and advancing citrus immunity engineering.
黄龙病(HLB)由亚洲韧皮杆菌(CLas)引起,是威胁全球柑橘生产的最具毁灭性的病害。尽管没有商业柑橘品种表现出对黄龙病的完全抗性,但基因型特异性的耐受性差异仍未得到充分研究。本研究对中国南方的六个商业柑橘品种进行了比较转录组分析,其中包括四个易感品种(本地早、贡柑、砂糖橘和纽荷尔脐橙)和两个耐病品种(尤力克柠檬;琯溪蜜柚),以剖析黄龙病响应的分子机制。比较转录组分析揭示了广泛的转录重编程,与易感基因型相比,耐病品种表现出较少的差异表达基因(DEGs)和靶向防御激活。关键发现突出了淀粉代谢的基因型特异性调控,其中β-淀粉酶3()在耐病品种中独特地上调,可能减轻淀粉积累。免疫信号传导有显著差异:耐病品种通过类受体激酶()激活模式触发免疫(PTI)并抑制与ROS相关的RBOH基因,而易感基因型则表现出乙烯信号传导和氧化应激途径的过度激活。易感品种的细胞壁重塑涉及木葡聚糖内转糖基酶()的上调,而耐病的尤力克柠檬中则诱导果胶甲酯酶以进行结构强化。植物激素动态揭示了尤力克柠檬中SA介导的防御和NPR3/4抑制,而易感品种则优先选择乙烯/茉莉酸途径。这些发现描绘了柑橘与CLas相互作用中的基因型特异性策略,确定了、和细胞壁修饰因子是通过分子辅助选择培育抗黄龙病品种的关键靶点。本研究为理解宿主-病原体动态和推进柑橘免疫工程提供了基础框架。