A nonsense mutation in Brown Spotted Leaf 2 (BSL2) gene encoding a receptor-like cytoplasmic kinase confers enhanced disease resistance in rice.

Abstract

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 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 an ethyl methane sulfonate (EMS) mutagenesis. The bsl2-1 is characterized as a single recessive mutation, resulting from a G-to-A single base-pair alteration that converts tryptophan (Trp) to a premature stop codon. The 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. The BSL2 is expressed globally and is induced by phytohormones and pathogens in rice, which 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 bsl2-1. 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.