BRHIS1 suppresses rice innate immunity through binding to monoubiquitinated H2A and H2B variants.

In the absence of pathogen attack, organisms usually suppress immune responses to reduce the negative effects of disease resistance. Monoubiquitination of histone variants at specific gene loci is crucial for gene expression, but its involvement in the regulation of plant immunity remains unclear. Here, we show that a rice SWI/SNF2 ATPase gene BRHIS1 is downregulated in response to the rice blast fungal pathogen or to the defense-priming-inducing compound BIT (1,2-benzisothiazol-3(2h)-one,1, 1-dioxide). The BRHIS1-containing complex represses the expression of some disease defense-related genes, including the pathogenesis-related gene OsPBZc and the leucine-rich-repeat (LRR) receptor-like protein kinase gene OsSIRK1. This is achieved through BRHIS1 recruitment to the promoter regions of target genes through specific interaction with monoubiquitinated histone variants H2B.7 and H2A.Xa/H2A.Xb/H2A.3, in the absence of pathogen attack or BIT treatment. Our results show that rice disease defense genes are initially organized in an expression-ready state by specific monoubiquitination of H2A and H2B variants deposited on their promoter regions, but are kept suppressed by the BRHIS1 complex, facilitating the prompt initiation of innate immune responses in response to infection through the stringent regulation of BRHIS1.