Chen Xinyu, Zhou Yujie, Liang Weifang, Zhou Yuhang, Xie Liujie, Hou Fan, Zheng Bingsong, Li Jianzhong
College of Plant Protection, Shenyang Agricultural University, Shenyang, China.
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Key Laboratory of Biotechnology in Plant Protection of MOA of China and Zhejiang Province, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Science, Hangzhou, China.
Front Plant Sci. 2025 Aug 28;16:1652068. doi: 10.3389/fpls.2025.1652068. eCollection 2025.
Most rice mutants exhibit some level of resistance to bacterial blight. This study demonstrates that the rice lesion mimic mutant (LMM) possesses enhanced resistance to bacterial leaf blight and triggers the upregulation of multiple pathogenesis-related (PR) proteins. Concurrently, photosynthetic parameter measurements revealed a significant impairment in the photosynthetic electron transport chain and photosynthetic capacity in pir1. Assessments of various stress factors and electron microscopy observations indicated that accumulated reactive oxygen species (ROS) caused severe damage to plant organelles. Utilizing proteomic approaches, we analyzed differentially expressed proteins (DEPs) between and its wild-type counterpart. Two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) combined with mass spectrometry (MS) analysis of different leaf positions from both materials identified a total of 321 DEPs, comprising 87 upregulated and 234 downregulated proteins. Bioinformatics analysis of these DEPs revealed their involvement in diverse biological processes, including photosynthesis, carbohydrate metabolism, defense responses, redox homeostasis, and energy metabolism. Analysis of the regulatory network suggests that the mutation participates in programmed cell death (PCD), thereby triggering disease resistance responses.
大多数水稻突变体对白叶枯病表现出一定程度的抗性。本研究表明，水稻病斑模拟突变体（LMM）对白叶枯病具有增强的抗性，并引发多种病程相关（PR）蛋白的上调。同时，光合参数测量显示pir1的光合电子传递链和光合能力有显著损伤。对各种胁迫因子的评估和电子显微镜观察表明，积累的活性氧（ROS）对植物细胞器造成了严重损伤。利用蛋白质组学方法，我们分析了pir1与其野生型对应物之间的差异表达蛋白（DEP）。二维荧光差异凝胶电泳（2D-DIGE）结合两种材料不同叶位的质谱（MS）分析共鉴定出321个DEP，包括87个上调蛋白和234个下调蛋白。对这些DEP的生物信息学分析揭示了它们参与多种生物学过程，包括光合作用、碳水化合物代谢、防御反应、氧化还原稳态和能量代谢。调控网络分析表明，pir1突变参与程序性细胞死亡（PCD），从而引发抗病反应。
