Polycomb repressive complex 2 (PRC2) contributes to catalyze the methylation of histone H3 at lysine 27 and plays vital roles in transcriptional silencing and growth development in various organisms. In Magnaporthe oryzae, histone H3K27 is found to associate with altered transcription of in planta induced genes. However, it is still unknown whether and how H3K27me3 modification is involved in pathogenicity to rice and stress response. In this study, we found that core subunits of PRC2, Kmt6-Suz12-Eed, were required for fungal pathogenicity to rice in M. oryzae. Kmt6-Suz12-Eed localized in the nuclei and was necessary for the establishment of H3K27me3 modification. With ChIP-seq analysis, 9.0% of genome regions enriched with H3K27me3 occupancy, which corresponded to 1033 genes in M. oryzae. Furthermore, deletion of Kmt6, Suz12 or Eed altered genome-wide transcriptional expression, while the de-repression genes in the ∆kmt6 strain were highly associated with H3K27me3 occupancy. Notably, plenty of genes which encode effectors and secreted enzymes, secondary metabolite synthesis genes, and cell wall stress-responsive genes were directly occupied with H3K27me3 modification and de-repression in the ∆kmt6 strain. These results elaborately explained how PRC2 was required for pathogenicity, which is closely related to effector modulated host immunity and host environment adaption.
