A nonsense mutation in the Brown Spotted Leaf 2 gene encoding a receptor-like cytoplasmic kinase confers enhanced disease resistance in rice

Receptor-like cytoplasmic kinases (RLCKs) are critical components that facilitate the connection between transmembrane-localized pattern recognition receptors (PRRs) and downstream signaling pathways involved in defense responses in plants. In this study, we present findings regarding the Brown Spotted Leaf 2 (BSL2) gene, which encodes a protein kinase in the RLCK superfamily, and its role in cell death-mediated defense responses in rice. We obtained a mutant exhibiting a lesion leaf phenotype, designated as brown spotted leaf 2-1 (bsl2-1), through ethylmethane sulfonate (EMS) mutagenesis. The bsl2-1 mutant is characterized as a single recessive mutation, resulting from a G-to-A single base pair alteration that converts tryptophan to a premature stop codon. BSL2 encodes a protein kinase containing a protein kinase catalytic (PKc) domain and a tight adherence D (TadD) domain. The bsl2-1 mutation disrupts the TadD domain, leading to the manifestation of a spontaneous lesion leaf phenotype. BSL2, which is expressed globally and is induced by phytohormones and pathogens in rice, encodes a protein localized in the cytoplasm. Histochemical analysis indicated a significant accumulation of reactive oxygen species, increased DNA fragmentation, and the occurrence of programmed cell death, generating a phenotype resembling a hypersensitive response in the bsl2-1 mutant. Furthermore, the bsl2-1 mutation conferred enhanced resistance to sheath blight and bacterial blight diseases. These findings suggest that BSL2 is involved in regulating innate immune responses and disease resistance in rice.