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BRHIS 1 suppresses rice innate immunity through binding to monoubiquitinated H2A and H2B variants
Author(s) -
Li Xiaoyu,
Jiang Yanxiang,
Ji Zhicheng,
Liu Yaoguang,
Zhang Qunyu
Publication year - 2015
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201440000
Subject(s) - innate immune system , biology , immunity , microbiology and biotechnology , genetics , immune system
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 / SNF 2 ATP ase 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 BRHIS 1‐containing complex represses the expression of some disease defense‐related genes, including the pathogenesis‐related gene Os PBZ c and the leucine‐rich‐repeat ( LRR ) receptor‐like protein kinase gene Os SIRK 1 . This is achieved through BRHIS 1 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 BRHIS 1 complex, facilitating the prompt initiation of innate immune responses in response to infection through the stringent regulation of BRHIS 1.