背景:黑麦(SecalegraineL.)是一种对环境压力具有高度耐受性的谷类作物,包括非生物和生物胁迫(例如,真菌疾病)。在这些真菌疾病中,叶锈病(LR)是黑麦生产的主要威胁。尽管进行了广泛的研究,黑麦对LR免疫反应的遗传基础尚不清楚.
结果:进行了RNA-seq分析,以检查三个无关的黑麦自交系(D33,D39和L318)感染了相容和不相容的Pucciniarereconditafsp的免疫反应。secalis(Prs)分离株。总的来说,在处理后20和36小时(hpt)鉴定了877个独特的差异表达基因(DEGs)。大多数DEG被上调。两个品系(D39和L318)的上调基因多于下调基因,而对于D33线观察到相反的趋势。DEGs的功能分类有助于鉴定受LR调控的最大基因群。值得注意的是,这些组包括几个编码细胞色素P450,受体样激酶,甲基酯酶,发病相关蛋白-1,木葡聚糖内葡萄糖基转移酶/水解酶,和过氧化物酶。代谢组学反应在基因型中高度保守,行D33在次级代谢产物中显示出最基因型特异性的变化。病原体相容性对代谢组学变化的影响小于时间点和基因型的影响。因此,黑麦的次级代谢组是通过识别病原体而不是成功感染而改变的。DEGs和差异积累的代谢物(DAMs)的富集分析结果反映了苯丙素和二萜生物合成以及硫胺素代谢参与黑麦免疫反应。
结论:我们的工作为黑麦对LR的遗传和代谢反应提供了新的见解。许多免疫反应相关的DEGs和DAMs被鉴定,从而阐明了在LR发育的早期阶段,黑麦对相容和不相容的Prs分离株的反应机制。转录组学和代谢组学分析的整合阐明了苯丙素生物合成和类黄酮途径对黑麦对Prs的免疫反应的贡献。组学数据的这种组合分析提供了与未来研究相关的有价值的见解,以增强黑麦对LR的抗性。
BACKGROUND: Rye (Secale cereale L.) is a cereal crop highly tolerant to environmental stresses, including abiotic and biotic stresses (e.g., fungal diseases). Among these fungal diseases, leaf rust (LR) is a major threat to rye production. Despite extensive research, the genetic basis of the rye immune response to LR remains unclear.
RESULTS: An RNA-seq analysis was conducted to examine the immune response of three unrelated rye inbred lines (D33, D39, and L318) infected with compatible and incompatible Puccinia recondita f. sp. secalis (Prs) isolates. In total, 877 unique differentially expressed genes (DEGs) were identified at 20 and 36 h post-treatment (hpt). Most of the DEGs were up-regulated. Two lines (D39 and L318) had more up-regulated genes than down-regulated genes, whereas the opposite trend was observed for line D33. The functional classification of the DEGs helped identify the largest gene groups regulated by LR. Notably, these groups included several DEGs encoding cytochrome P450, receptor-like kinases, methylesterases, pathogenesis-related protein-1, xyloglucan endotransglucosylases/hydrolases, and peroxidases. The metabolomic response was highly conserved among the genotypes, with line D33 displaying the most genotype-specific changes in secondary metabolites. The effect of pathogen compatibility on metabolomic changes was less than the effects of the time-points and genotypes. Accordingly, the secondary metabolome of rye is altered by the recognition of the pathogen rather than by a successful infection. The results of the enrichment analysis of the DEGs and differentially accumulated metabolites (DAMs) reflected the involvement of phenylpropanoid and diterpenoid biosynthesis as well as thiamine metabolism in the rye immune response.
CONCLUSIONS: Our work provides novel insights into the genetic and metabolic responses of rye to LR. Numerous immune response-related DEGs and DAMs were identified, thereby clarifying the mechanisms underlying the rye response to compatible and incompatible Prs isolates during the early stages of LR development. The integration of transcriptomic and metabolomic analyses elucidated the contributions of phenylpropanoid biosynthesis and flavonoid pathways to the rye immune response to Prs. This combined analysis of omics data provides valuable insights relevant for future research conducted to enhance rye resistance to LR.