Abstract
Epigenetic modifications involve complex and sophisticated control over chromatin states and DNA methylation patterns, which are important for stress tolerance in plants. While the identification of epigenetic modulating enzymes keeps growing, such as MET1, for CG methylation; CMT3, DRM2, DRM3 for CHH methylation; and IBM1, SUVH4 for CHG methylation; the molecular roles of these regulators in specific physiological functions remain obscure. In a mutant screen, we identified IBM1 as a new player in plant immunity. The ibm1 mutants were hyper-susceptible to hemi-biotrophic bacteria Pseudomonas syringae. Accordingly, bacteria-induced up-regulation of PR1, PR2, and FRK1 defense markers was abolished in ibm1 mutants. Consistently, at the chromatin level, these defense marker genes showed enrichment of the inactivation mark, H3K9me2; while the activation mark H3K4me3 was reduced in ibm1 mutants. Immunoprecipitation of associated chromatin further demonstrated that IBM1 binds directly to the gene body of PR1, PR2, and FRK1. Taken together, these data suggest that IBM1 plays a critical role in modulating Arabidopsis immunity through direct regulation of defense gene expression. Notably, IBM1 maintains a permissive chromatin environment to ensure proper induction of defense genes under some biotic stress.
Highlights
Epigenetic control of the plant immunity response provides plasticity for the dynamic regulation of emerging pathogens, and at the same time maintains genome stability to avoid the generation of genomic lesion (Fu and Dong, 2013; Espinas et al, 2016)
In a screen to evaluate whether epigenetic regulators such as IN BONSAI METHYLATION 1 (IBM1), met1, cmt3, drm1, drm2, drm3, ddm1, and hac1 are involved in Arabidopsis immunity to bacteria, mutants were dip-inoculated with virulent, hemi-biotrophic bacteria Pst DC3000 and disease symptoms were compared to respective wild-type (WT)
This work shows that IBM1 is required for Arabidopsis full resistance to Pst DC3000 infection
Summary
Epigenetic control of the plant immunity response provides plasticity for the dynamic regulation of emerging pathogens, and at the same time maintains genome stability to avoid the generation of genomic lesion (Fu and Dong, 2013; Espinas et al, 2016). The plant defense response against biotrophic pathogens is mediated by salicylic acid (SA)-dependent signaling, while signals for resistance to necrotrophs occur through the jasmonic acid/ethylene (JA/ET) pathway (Katagiri et al, 2002; Alvarez et al, 2010). Depending on the concentration of SA and JA, the two pathways can work synergistically or antagonize each other (Koornneef and Pieterse, 2008; Bari and Jones, 2009; Vlot et al, 2009). Both signaling cascades converge at the expression of antimicrobial pathogenesisrelated (PR) genes in local environment as well as in distal tissue for long-term protection
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