Liang Dong, Qi Zhongqiang, Du Yan, Yu Junjie, Yu Mina, Zhang Rongsheng, Cao Huijuan, Pan Xiayan, Qiao Junqing, Song Tianqiao, Liu Youzhou, Chen Zhiyi, Liu Yongfeng
Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences (JAAS), Nanjing, China.
Front Plant Sci. 2022 Apr 5;13:723356. doi: 10.3389/fpls.2022.723356. eCollection 2022.
causes rice blast disease and is responsible for major losses in rice production worldwide. Although numerous studies have focused on the interactions between and , to date, the conserved mechanisms remain in part unclear. In this study, a comparative analysis of transcriptomes of L. ssp. cv. 'Nipponbare' interacting with three strains (248, 235, and 163) were performed to explore the conserved molecular mechanisms. Differentially expressed genes with similar expression patterns in the interactions between cultivar 'Nipponbare' and three strains were defined as Conserved Differentially Expressed Genes (CDEGs). These included 3,647 CDEGs and 3,655 CDEGs. Four rice CDEGs (, , , and ) encoding universal stress protein (USP) were induced within 24 h post-inoculation (hpi) by three strains. Meanwhile, overexpression of resulted in enhanced rice resistance against . Furthermore, four rice genes coding light-harvesting chlorophyll a/b-binding (LHC) protein (, , , ) were also identified as CDEGs and were induced at 48 hpi, which might contribute to blast resistance through reactive oxygen species (ROS) accumulation. is effector inducing rice cell death and were verified that include AA9 CAZy domain (namely GH61 domain). In this study, we found seven homologous genes coding proteins with signal peptides and AA9 CAZy domains, which were continuously up-regulated across all infection stages relative to uninoculated control. This study uncovered that genes are required for conserved mechanisms of rice- interaction, which includes rice genes encoding USP proteins and LHC proteins, as well as genes encoding AA9 proteins. This study will help us to understand how responds to infections and the molecular mechanisms of pathogenicity.
引起稻瘟病,导致全球水稻产量大幅损失。尽管众多研究聚焦于[病原菌名称]与[水稻品种名称]之间的相互作用,但迄今为止,保守机制仍部分不明。本研究对[水稻品种名称]与三个[病原菌名称]菌株(248、235和163)相互作用的转录组进行了比较分析,以探索保守的分子机制。在品种‘日本晴’与三个[病原菌名称]菌株的相互作用中,具有相似表达模式的差异表达基因被定义为保守差异表达基因(CDEGs)。其中包括3647个[水稻品种名称]CDEGs和3655个[病原菌名称]CDEGs。三个[病原菌名称]菌株在接种后24小时内诱导了四个编码通用应激蛋白(USP)的水稻CDEGs([基因名称1]、[基因名称2]、[基因名称3]和[基因名称4])。同时,[基因名称]的过表达导致水稻对[病原菌名称]的抗性增强。此外,四个编码光捕获叶绿素a/b结合(LHC)蛋白的水稻基因([基因名称5]、[基因名称6]、[基因名称7]、[基因名称8])也被鉴定为CDEGs,并在接种后48小时被诱导,这可能通过活性氧(ROS)积累促进稻瘟病抗性。[效应因子名称]是诱导水稻细胞死亡的效应因子,已证实其包含AA9碳水化合物活性酶结构域(即GH61结构域)。在本研究中,我们发现了七个编码具有信号肽和AA9碳水化合物活性酶结构域蛋白的同源基因,相对于未接种对照,它们在所有感染阶段均持续上调。本研究揭示了[病原菌名称]与水稻相互作用的保守机制所需的基因,包括编码USP蛋白和LHC蛋白的水稻基因,以及编码AA9蛋白的[病原菌名称]基因。本研究将有助于我们了解[病原菌名称]如何应对[水稻品种名称]感染以及[病原菌名称]致病的分子机制。