Molecular and physiological interplay between Rhizoctonia solani pathogenesis and rice defence: Recent advances and future outlook

Rice sheath blight, caused by the necrotrophic fungus Rhizoctonia solani, remains a major constraint on global rice production, affecting 15–20 million hectares annually and causing yield losses of up to 50 % under epidemic conditions. The pathogen's broad host range, extensive genetic and pathogenic variability and the absence of durable host resistance make disease management particularly challenging. Rhizoctonia solani induces host tissue necrosis through cell wall-degrading enzymes, toxins, oxalic acid and effector molecules, disrupting photosynthesis, oxidative balance and carbon metabolism. In response, rice deploys a multilayered defence network involving pattern recognition receptors, jasmonic acid and ethylene mediated signalling, redox homeostasis, transcriptional reprogramming and cell wall reinforcement, reflecting the dynamic interplay between pathogen aggressiveness and host defence that determines disease outcome. Genetic studies have identified over 100 quantitative trait loci linked to sheath blight resistance and functional analyses have revealed key resistance-associated genes, such as SBRR1-R from indica germplasm, a promising candidate for molecular breeding that still awaits functional validation and field-level confirmation across diverse genetic backgrounds. Building on this foundation, emerging strategies including clustered regularly interspaced short palindromic repeats/CRISPR-associated (CRISPR/Cas) based engineering of susceptibility genes, host-induced gene silencing, defence priming, beneficial microbe-mediated induced systemic resistance and genome-assisted breeding offer environmentally sustainable avenues for durable disease management. This review synthesises recent advances in the molecular and physiological mechanisms underlying the rice-R. solani pathosystem and outlines emerging strategies for engineering durable sheath blight resistance.