LAUSR

Rhizoctonia solani causes sheath blight disease in rice; however, the defense mechanism of rice plants against R. solani remains elusive. To analyze the roles of brassinosteroid (BR) and ethylene signaling on rice defense to R. solani, wild-type (WT) rice and several mutants and overexpressing (OX) lines were inoculated with R. solani. Mutants d61-1 and d2 were less susceptible to sheath blight disease, bri1-D was more susceptible, and ravl1 and d61-1/EIL1 Ri5 were similarly susceptible compared with WT. The double mutant ravl1/d61-1 was phenotypically similar to the ravl1 mutant. Transcriptome analysis, chromatin immunoprecipitation assay, electrophoretic mobility shift assay, and transient assays indicted that RAVL1 might directly activate Ethylene insensitive 3-like 1 (EIL1), a master regulator of ethylene signaling. Mutants ers1 and d61-1/RAVL1 OX were resistant to sheath blight disease, whereas EIL1 RNAi mutants and RAVL1 OX were more susceptible than WT. BRI1 and D2 expression in EIL1 Ri5/RAVL1 OX and EIL1 expression in d61-1/RAVL1 OX indicated that RAVL1 activates BRI1/D2 and EIL1, respectively, independent of BR and ethylene signaling. Our analyses provide information on how BR and ethylene signaling regulate sheath blight disease and on the regulatory function of RAVL1 in rice sheath blight disease.