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Investigation of the role of histone modification propagating activity of GLP

ABSTRACT: We use ChIP-Seq and RNA-Seq technology to profile the H3K9me2 modification and transcription under different conditions of GLP activity. GLP and G9a are major H3K9 dimethylases, and are essential for mouse early embryonic development. Here we report that GLP and G9a possess intrinsic histone methylation propagating activities. The histone methyltransferase activities of GLP and G9a are stimulated by neighboring nucleosomes pre-methylated at H3K9. These stimulation events function in cis and are dependent on H3K9 methylation binding activities of ankyrin repeats domains in GLP and G9a. In mouse embryonic stem cells (ESCs) harboring a mutant GLP lacking H3K9 methylation propagating activity, pluripotent genes display a delayed kinetics in establishing H3K9 methylation and gene silencing during differentiation. Disruption of the H3K9 methylation propagating activity of GLP in mice causes growth retardation of the embryos, ossification defects of calvaria and early postnatal lethality. We propose that GLP¡¯s ability to rapidly propagate H3K9 methylation is required for efficient gene silencing during programmed cell fate transition.

ORGANISM(S): Mus musculus

PROVIDER: GSE54412 | GEO | 2015/01/20

REPOSITORIES: GEO

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Investigation of the role of histone modification propagating activity of GLP

Project description:We use ChIP-Seq and RNA-Seq technology to profile the H3K9me2 modification and transcription under different conditions of GLP activity. GLP and G9a are major H3K9 dimethylases, and are essential for mouse early embryonic development. Here we report that GLP and G9a possess intrinsic histone methylation propagating activities. The histone methyltransferase activities of GLP and G9a are stimulated by neighboring nucleosomes pre-methylated at H3K9. These stimulation events function in cis and are dependent on H3K9 methylation binding activities of ankyrin repeats domains in GLP and G9a. In mouse embryonic stem cells (ESCs) harboring a mutant GLP lacking H3K9 methylation propagating activity, pluripotent genes display a delayed kinetics in establishing H3K9 methylation and gene silencing during differentiation. Disruption of the H3K9 methylation propagating activity of GLP in mice causes growth retardation of the embryos, ossification defects of calvaria and early postnatal lethality. We propose that GLP¡¯s ability to rapidly propagate H3K9 methylation is required for efficient gene silencing during programmed cell fate transition. H3K9me2 and H3K9me1 are ChIPped and sequenced in WT mESC and GLP-mutant mESCs, and RNA-Seq was done for those cells as well.

2015-01-20 | E-GEOD-54412 | biostudies-arrayexpress

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The Histone H3 Lysine 9 Methyltransferases G9a and GLP Regulate Polycomb Repressive Complex 2-Mediated Gene Silencing [Affymetrix]

Project description:G9a/GLP and Polycomb Repressive Complex 2 (PRC2) are two major epigenetic silencing machineries, which in particular methylate histone H3 on lysines 9 and 27 (H3K9 and H3K27), respectively. Although evidence of a crosstalk between H3K9 and H3K27 methylations has started to emerge, their actual interplay remains elusive. Here, we show that PRC2 and G9a/GLP interact physically and functionally. Moreover, combining different genome-wide approaches, we demonstrate that Ezh2 and G9a/GLP share an important number of common genomic targets, encoding developmental and neuronal regulators. Furthermore, we show that G9a enzymatic activity modulates PRC2 genomic recruitment to a subset of its target genes. Taken together, our findings demonstrate an unanticipated interplay between two main histone lysine methylation mechanisms, which cooperate to maintain silencing of a subset of developmental genes. Microarray has been perform in triplicate on total extract RNA from mES cell (TT2 : Wildtype and KOs G9a-/-, GLP-/-, G9a-/- and GLP-/-)

2014-01-03 | E-GEOD-46544 | biostudies-arrayexpress

The Histone H3 Lysine 9 Methyltransferases G9a and GLP Regulate Polycomb Repressive Complex 2-Mediated Gene Silencing [ChIP-Seq]

Project description:G9a/GLP and Polycomb Repressive Complex 2 (PRC2) are two major epigenetic silencing machineries, which in particular methylate histone H3 on lysines 9 and 27 (H3K9 and H3K27), respectively. Although evidence of a crosstalk between H3K9 and H3K27 methylations has started to emerge, their actual interplay remains elusive. Here, we show that PRC2 and G9a/GLP interact physically and functionally. Moreover, combining different genome-wide approaches, we demonstrate that Ezh2 and G9a/GLP share an important number of common genomic targets, encoding developmental and neuronal regulators. Furthermore, we show that G9a enzymatic activity modulates PRC2 genomic recruitment to a subset of its target genes. Taken together, our findings demonstrate an unanticipated interplay between two main histone lysine methylation mechanisms, which cooperate to maintain silencing of a subset of developmental genes. ChIP-seq has been performed for G9a and Ezh2 in wild type TT2 mES cells or in mES cells lacking both G9a and GLP (G9a-/-GLP-/-). As a control, input DNA was saved before immunoprecipitation. Note that the two inputs (Input_TT2_0 and Input_TT2_1) have been combined and used as control for Ezh2 and G9a ChIP-seq.

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The Histone H3 Lysine 9 Methyltransferases G9a and GLP Regulate Polycomb Repressive Complex 2-Mediated Gene Silencing [RNA-Seq]

Project description:G9a/GLP and Polycomb Repressive Complex 2 (PRC2) are two major epigenetic silencing machineries, which in particular methylate histone H3 on lysines 9 and 27 (H3K9 and H3K27), respectively. Although evidence of a crosstalk between H3K9 and H3K27 methylations has started to emerge, their actual interplay remains elusive. Here, we show that PRC2 and G9a/GLP interact physically and functionally. Moreover, combining different genome-wide approaches, we demonstrate that Ezh2 and G9a/GLP share an important number of common genomic targets, encoding developmental and neuronal regulators. Furthermore, we show that G9a enzymatic activity modulates PRC2 genomic recruitment to a subset of its target genes. Taken together, our findings demonstrate an unanticipated interplay between two main histone lysine methylation mechanisms, which cooperate to maintain silencing of a subset of developmental genes. RNA-seq has been perform in triplicate on mES cell (TT2 : Wildtype, and KO G9a-/-)

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The Histone H3 Lysine 9 Methyltransferases G9a and GLP Regulate Polycomb Repressive Complex 2-Mediated Gene Silencing [RNA-Seq]

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The Histone H3 Lysine 9 Methyltransferases G9a and GLP Regulate Polycomb Repressive Complex 2-Mediated Gene Silencing [ChIP-Seq]

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Complete loss of H3K9 methylation dissolves mouse heterochromatin organization

Project description:Histone H3 lysine 9 (H3K9) methylation is a central epigenetic modification that defines heterochromatin from unicellular to multicellular organisms. In mammalian cells, H3K9 methylation can be catalyzed by at least six distinct SET domain enzymes: Suv39h1/Suv39h2, Eset1/Eset2 and G9a/Glp. We used mouse embryonic fibroblasts (MEFs) with a conditional mutation for Eset1 and introduced progressive deletions for the other SET domain genes by CRISPR/Cas9 technology. Compound mutant MEFs for all 6 SET domain methyltransferase (KMT) genes lack all H3K9 methylation states, derepress nearly all families of repeat elements and display genomic instabilities. Strikingly, the 6KO H3K9 KMT MEFs no longer maintain heterochromatin organization and have lost electron-dense heterochromatin. This is the first analysis of H3K9 methylation deficient mammalian chromatin and reveals a crucial function for H3K9 methylation in protecting heterochromatin organization and genome integrity.

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