肉桂疫霉Rands破坏了全世界的森林物种,造成重大的生态和经济影响。欧洲栗子(Castaneasativa)对这种半生营养卵菌敏感,而亚洲栗子(板栗和板栗)具有抗性,并已成功用作育种计划中的抗性供体。板栗物种之间不同疾病结果的分子机制是制定基于科学的控制策略的关键基础。然而,这些仍然知之甚少。在用肉桂P接种的紫花苜蓿和肉芽菜根中进行双重RNA测序。研究的时间点代表了先前在细胞水平上描述的病原体的半营养生活方式。肉桂疫霉在两个栗种中表达了几个与致病性相关的基因,如细胞壁降解酶,宿主营养吸收转运蛋白,和效应器。然而,在易感栗中,与宿主程序性细胞死亡(elicitins和NLP)和孢子形成相关基因有关的效应子的表达较高。病原体接种后,1,556和488个基因在C.crenata和C.sativa中差异表达,分别。最显着的转录变化发生在接种后2小时(hai),在C.crenata中发生48hai。然而,C.crenata诱导更多的防御相关基因,表明对肉桂的抗性反应由多个基因座控制,包括几个模式识别受体,涉及苯丙素的基因,水杨酸和乙烯/茉莉酸途径,和抗真菌基因。重要的是,这些结果验证了先前观察到的C.crenata的细胞反应。总的来说,这项研究提供了一个全面的时间分辨的板栗的描述。肉桂动态,揭示了易感和抗性宿主反应以及与疾病发展有关的重要病原体策略的新见解。
Phytophthora cinnamomi Rands devastates forest species worldwide, causing significant ecological and economic impacts. The European chestnut (Castanea sativa) is susceptible to this hemibiotrophic
oomycete, whereas the Asian chestnuts (Castanea crenata and Castanea mollissima) are resistant and have been successfully used as resistance donors in breeding programs. The molecular mechanisms underlying the different disease outcomes among chestnut species are a key foundation for developing science-based control strategies. However, these are still poorly understood. Dual RNA sequencing was performed in C. sativa and C. crenata roots inoculated with P. cinnamomi. The studied time points represent the pathogen\'s hemibiotrophic lifestyle previously described at the cellular level. Phytophthora cinnamomi expressed several genes related to pathogenicity in both chestnut species, such as cell wall-degrading enzymes, host nutrient uptake transporters, and effectors. However, the expression of effectors related to the modulation of host programmed cell death (elicitins and NLPs) and sporulation-related genes was higher in the susceptible chestnut. After pathogen inoculation, 1,556 and 488 genes were differentially expressed by C. crenata and C. sativa, respectively. The most significant transcriptional changes occur at 2 h after inoculation (hai) in C. sativa and 48 hai in C. crenata. Nevertheless, C. crenata induced more defense-related genes, indicating that the resistant response to P. cinnamomi is controlled by multiple loci, including several pattern recognition receptors, genes involved in the phenylpropanoid, salicylic acid and ethylene/jasmonic acid pathways, and antifungal genes. Importantly, these results validate previously observed cellular responses for C. crenata. Collectively, this study provides a comprehensive time-resolved description of the chestnut-P. cinnamomi dynamic, revealing new insights into susceptible and resistant host responses and important pathogen strategies involved in disease development.