Genome-wide mapping of H3K27 tri-methylation in PRC2 components of Pyricularia oryzae

We report different roles of three PRC2 components, KMT6, P55 and SIN3 played in distribution of genome-wide H3K27 tri-methylation of Pyricularia oryzae. Polycomb repressive complex 2 (PRC2), which is composed of Ezh(Kmt6), Su(z)12, Esc(Eed) and accessory subunits RbAp48/Nurf55(P55), catalyzes the methylation of histone H3 at lysine 27. Loss of P55 caused severe global defects in the normal distribution of H3K27me3 and transcriptional reprogramming on the H3K27me3-occupied genes. Furthermore, we found that the Sin3 histone deacetylase complex was required to sustain H3K27me3 occupancy and stably maintain gene repression by directly interacting with P55. Examination of H3K27 tri-methylation of different PRC2 components of Pyricularia oryzae. Two biological replicates were performed.

本研究解析了稻瘟病菌（Pyricularia oryzae）中3种多梳抑制复合体2（Polycomb repressive complex 2, PRC2）组分——KMT6、P55与SIN3在全基因组H3K27三甲基化（H3K27 tri-methylation）分布中的调控作用。多梳抑制复合体2（PRC2）由Ezh(Kmt6)、Su(z)12、Esc(Eed)及辅助亚基RbAp48/Nurf55(P55)构成，可催化组蛋白H3第27位赖氨酸的甲基化修饰。缺失P55会导致H3K27me3的正常分布出现严重的全局性缺陷，并引发H3K27me3靶标基因的转录重编程。此外，本研究发现SIN3组蛋白去乙酰化酶复合体（Sin3 histone deacetylase complex）可通过直接与P55相互作用，维持H3K27me3的染色质占据水平，并稳定维持靶基因的转录抑制状态。本研究针对稻瘟病菌不同PRC2组分的H3K27三甲基化水平开展了检测，共设置2次生物学重复。