Differential proteomic analysis reveals key players in rice resistance to Rhizoctonia solani pathogenesis

Rhizoctonia solani is a necrotrophic fungus that causes sheath blight (ShB) in rice, resulting in substantial yield losses. A major challenge in managing this disease is the lack of fully resistant rice varieties. While some germplasms show partial resistance, the underlying mechanisms remain poorly understood. In this study, we used quantitative proteomics to investigate host-pathogen interactions and identify differentially abundant proteins (DAPs) in response to R. solani infection. Label-free quantitative proteomics (LC-MS/MS) was employed to compare the proteomes of the moderately resistant variety CR 1014 and the susceptible variety Swarna-Sub1, revealing 753, 681, 680, and 992 differentially abundant proteins (DAPs) at 12, 24, 48, and 72 h post-infection, respectively. Our results indicate that CR 1014 exhibits enhanced redox homeostasis, with a significant upregulation of reactive oxygen species (ROS)-scavenging proteins, such as peroxidases and glutathione S-transferases, compared to Swarna-Sub1. CR 1014 also demonstrated robust activation of carbohydrate metabolism, the phenylpropanoid pathway, and the quinate pathway-key processes involved in lignification and the synthesis of defense-related compounds. Additionally, pathogenesis-related proteins, such as chitinases and PR10 family members, were strongly induced in CR 1014, reinforcing its heightened defense response. In contrast, Swarna-Sub1 showed an insufficient induction of key defense enzymes like phenylalanine ammonia-lyase and chorismate mutase. Furthermore, its susceptibility was reflected in impaired photosynthesis and fatty acid metabolism. These findings provide valuable insights into the proteomic landscape of rice during R. solani infection and highlight potential targets for improving ShB resistance. This study establishes a framework for understanding the molecular mechanisms underlying resistance and susceptibility to this destructive pathogen.