Sun Xiaomeng, Zhang Ruiyu, Wang Zongping, Zhang Haotian, Wen Hairun, Zhang Junli, Yu Naibin, Wang Zhe, Tai Huanhuan, Yang Qin
State Key Laboratory of Crop Stress Resistance and High-Efficiency Production, College of Agronomy, Northwest A&F University, Yangling, China.
Hainan Research Institute of Northwest A&F University, Sanya, China.
Front Plant Sci. 2025 Jun 5;16:1580016. doi: 10.3389/fpls.2025.1580016. eCollection 2025.
Gray leaf spot (GLS), caused by and , is a devastating foliar disease affecting maize production worldwide. However, the defense mechanisms underlying GLS resistance are poorly understood. A major quantitative trait locus (QTL), , associated with GLS resistance, was previously identified on maize chromosome 8 bin 8.06. Here we conducted transcriptome analyses on leaves from a pair of B73-teosinte near-isogenic lines (NILs) with contrasting alleles infected with at 0, 4, 8, and 12 hours post inoculation (hpi). A total of 1225 up-regulated genes (URGs) were identified in the resistant line Qgls8-R compared with the susceptible line Qgls8-S across the four time points. By contrast, 908 URGs were identified in Qgls8-S. The URGs in Qgls8-R were significantly enriched in metabolic processes, phytohormone signaling, and response to biotic stress, while the URGs in Qgls8-S were mostly involved in plant growth and developmental processes. Additionally, -induced URGs were consistently enriched in terpenoid metabolism and jasmonic acid (JA) signaling. Terpene- and JA-related genes showed increased expression at least at one time point after infection which were confirmed by RT-qPCR. Furthermore, metabolite quantification indicated higher levels of JA and its isoleucine conjugate (JA-Ile) in Qgls8-R compared to Qgls8-S. Weighted gene co-expression network analysis (WGCNA) identified the module "turquoise", which exhibited the highest positive correlation with Qgls8-R and was related to JA signaling. These findings suggest that the defense response mediated by terpenoid metabolism and the JA signaling pathway plays crucial roles in enhancing GLS resistance following infection.
灰斑病(GLS)由[病原菌名称缺失]引起,是一种严重影响全球玉米生产的叶部病害。然而,人们对GLS抗性的防御机制了解甚少。先前在玉米第8染色体8.06 bin上鉴定出一个与GLS抗性相关的主要数量性状位点(QTL)[位点名称缺失]。在此,我们对一对B73 - 大刍草近等基因系(NILs)的叶片进行了转录组分析,这对近等基因系具有不同的[基因名称缺失]等位基因,在接种后0、4、8和12小时(hpi)接种[病原菌名称缺失]。在四个时间点上,与感病系Qgls8 - S相比,抗性系Qgls8 - R中共鉴定出1225个上调基因(URGs)。相比之下,Qgls8 - S中鉴定出908个URGs。Qgls8 - R中的URGs在代谢过程、植物激素信号传导和对生物胁迫的反应中显著富集,而Qgls8 - S中的URGs大多参与植物生长和发育过程。此外,[病原菌名称缺失]诱导的URGs在萜类代谢和茉莉酸(JA)信号传导中持续富集。萜类和JA相关基因在[病原菌名称缺失]感染后的至少一个时间点表达增加,这通过RT - qPCR得到证实。此外,代谢物定量表明,与Qgls8 - S相比,Qgls8 - R中JA及其异亮氨酸共轭物(JA - Ile)的水平更高。加权基因共表达网络分析(WGCNA)确定了“绿松石”模块,该模块与Qgls8 - R呈最高正相关且与JA信号传导有关。这些发现表明,萜类代谢和JA信号通路介导的防御反应在增强[病原菌名称缺失]感染后的GLS抗性中起关键作用。