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PFA Ependymoma-associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (RNA-seq)

ABSTRACT: To understand the EZHIP-mediated transcriptional profile in mouse embryonic fibroblasts

ORGANISM(S): Mus musculus

PROVIDER: GSE124839 | GEO | 2019/04/08

REPOSITORIES: GEO

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PFA ependymoma-associated protein EZHIP inhibits PRC2 activity through a H3 K27M-like mechanism.

Project description:Posterior fossa type A (PFA) ependymomas exhibit very low H3K27 methylation and express high levels of EZHIP (Enhancer of Zeste Homologs Inhibitory Protein, also termed CXORF67). Here we find that a conserved sequence in EZHIP is necessary and sufficient to inhibit PRC2 catalytic activity in vitro and in vivo. EZHIP directly contacts the active site of the EZH2 subunit in a mechanism similar to the H3 K27M oncohistone. Furthermore, expression of H3 K27M or EZHIP in cells promotes similar chromatin profiles: loss of broad H3K27me3 domains, but retention of H3K27me3 at CpG islands. We find that H3K27me3-mediated allosteric activation of PRC2 substantially increases the inhibition potential of EZHIP and H3 K27M, providing a mechanism to explain the observed loss of H3K27me3 spreading in tumors. Our data indicate that PFA ependymoma and DIPG are driven in part by the action of peptidyl PRC2 inhibitors, the K27M oncohistone and the EZHIP 'oncohistone-mimic', that dysregulate gene silencing to promote tumorigenesis.

| S-EPMC6513997 | biostudies-literature

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq Ring1b)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124741 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq H2K27me3)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124740 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq CBX2)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124739 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-04-08 | GSE124743 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism

Project description:Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism

| PRJNA513308 | ENA

PFA Ependymoma-associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (RNA-seq)

Project description:PFA Ependymoma-associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (RNA-seq)

| PRJNA513969 | ENA

H3 K27M and EZHIP impede H3K27-methylation spreading by inhibing allosterically stimulated PRC2 [EZHIP]

Project description:In this study, we report that EZHIP and H3 K27M preferentially interact with an allosterically activated form of PRC2 in vivo. The formation of H3 K27M- and EZHIP-PRC2 complexes occurs at CpG islands containing H3K27me3 and impedes PRC2 and H3K27me3 spreading. Moreover, we find that H3 K27M inhibits PRC2 in trans and can reduce H3K27me3 levels independent of chromatin incorporation. While EZHIP is not found outside of placental mammals, we find that expression of human EZHIP reduces H3K27me3 in Drosophila melanogaster through a conserved molecular mechanism.

2020-10-12 | GSE151979 | GEO

H3 K27M and EZHIP impede H3K27-methylation spreading by inhibing allosterically stimulated PRC2 [K27M]

2020-10-12 | GSE151980 | GEO

Histone H3 wild-type DIPG/DMG overexpressing EZHIP extend the spectrum diffuse midline gliomas with PRC2 inhibition beyond H3-K27M mutation

Project description:Characterisation of a new subgroup of DMG lacking H3-K27M mutation that is defined by H3K27me3 loss and EZHIP overexpression that can be detected by IHC. These tumors are distinct from EZHIP-positive posterior fossa ependymomas and are associated with a dismal prognosis. We propose that these EZHIP/H3-WT tumors need to be considered similar to canonical DIPG/DMG, thus extending the spectrum of DMG with PRC2 inhibition beyond H3-K27M mutation

2020-03-20 | E-MTAB-8888 | biostudies-arrayexpress

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