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Bivalent histone modification of BCG1 enables fungal pathogen to evade host immunity (RNA-Seq)

ABSTRACT: Bivalent chromatin modification containing opposing H3K4me3 and H3K27me3 marks controls various biological processes by fine-tuning gene expression in animals and plants, however how this bivalent modification regulates pathogenicity of fungal pathogen remains exclusive. Here, we provided a genome-wide landscape of H3K4me3 and H3K27me3 of wheat head blight fungus Fusarium graminearum (Fg), leading to the identification of infection-induced bivalent chromatin-marked genes (BCGs). Among those, BCG1, which encodes a novel xylanase with a G/Q rich motif, is required for the full virulence of Fg pathogenicity through degradation of host cell wall. However, the G/Q rich motif is recognized by pattern-recognition receptors and triggers plant innate immunity. Further data illustrates that Fg employs H3K4me3 modification to induce BCG1 expression rapidly during the early infection, and then switches to bivalent H3K4me3-H3K27me3 chromatin state that renders rapid epigenetic silencing of BCG1 for escaping from host immune monitor, therefore leading to the successful invasion. Collectively, our study highlights the molecular mechanism of how fungal pathogen employs bivalent epigenetic modification to facilitate the successful infection by escaping of host immunity, which provides conceptual insights into plant-microbe interaction.

ORGANISM(S): Fusarium graminearum PH-1 Triticum aestivum

PROVIDER: GSE213960 | GEO | 2023/12/04

REPOSITORIES: GEO

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Bivalent histone modification of BCG1 enables fungal pathogen to evade host immunity (RNA-Seq)

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