GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE304nnn/GSE304049/primaryOK200TranscriptomicsTriticum aestivumExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304049GEOGSEfalseH3K27me3-mediated epigenetic silencing of FgHMG1 enables fungal host immune evasionH3 lysine 27 trimethylation (H3K27me3) plays a role in the pathogenesis of pathogenic fungi, however, the molecular mechanisms underlying the dynamic regulation of functional gene expression by H3K27me3 modification to facilitate fungal invasion remain elusive. Here, we identified 132 H3K27me3 modification-marked genes (FgHMGs) via dynamic profiling of H3K27me3 modifications during Fusarium graminearum infection. Functional characterization revealed that FgHMG1 acts as a pathogen-associated molecular pattern (PAMP) to induce PAMP-triggered immunity (PTI) in Nicotiana benthamiana independently of its enzymatic activity, with immune activation requiring the receptor kinases LRR-RLK BAK1 and SOBIR1. In addition, FgHMG1 also induced ROS accumulation, upregulated defense genes. Notably, FgHMG1 transcription was suppressed during infection via H3K27me3 deposition mediated by histone methyltransferase FgKMT6. Genetic disruption of FgKMT6 abolished H3K27me3 enrichment, derepressing FgHMG1 and elevating host immunity. This immune response was markedly attenuated in ΔFgKMT6-FgHMG1 double mutants, confirming FgKMT6-dependent epigenetic suppression of FgHMG1 as a critical virulence strategy. In 2-year field trials, foliar pretreatment with either FgHMG1 protein reduced Fusarium head blight in wheat by 35–50%, demonstrating their potential as elicitors for managing this disease. Collectively, these findings elucidate how fungal pathogens exploit H3K27me3 plasticity to fine-tune PAMP expression, enabling adaptive immune evasion during host colonization.2026/05/15GSE304049GSM9141740GSM9141742GSM9141741GSM9141737GSM9141739GSM914173823509304049Triticum aestivum[41493395]