MTF2 and JARID2 function in ESC differentiation
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ABSTRACT:
PROVIDER: PRJNA656285 | ENA |
REPOSITORIES: ENA
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Project description:We performed mRNA-seq after differentiation of embryonic stem cells (ESCs) into cardiac precursors (CPs) with with or without inducing degradation of PRC2 subunits MTF2, JARID2, or SUZ12 using the AID system
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Project description:We performed mRNA-seq before and after differentiation of embryonic stem cells (ESCs) into neural progenitor cells (NPCs) with with or without inducing degradation of PRC2 subunits MTF2, JARID2, or SUZ12 using the AID system
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Project description:The Polycomb Group proteins foster gene repression profiles required for proper development and unimpaired adulthood, and comprise the components of the PRC2 complex including the histone H3 lysine 27 (H3K27) methyltransferase Ezh2. How mammalian PRC2 accesses chromatin is unclear. We find that Jarid2 associates with PRC2 and stimulates its enzymatic activity in vitro. Jarid2 contains a Jumonji C domain, but is devoid of detectable histone demethylase activity. Instead, its artificial recruitment to a promoter in vivo resulted in co-recruitment of PRC2 with resultant increased levels of H3K27me2/3. Jarid2 co-localizes with Ezh2 and MTF2, a homologue of Drosophila Pcl, at endogenous genes in ES cells. Jarid2 can itself bind DNA and its recruitment in ES cells is interdependent with that of PRC2 as Jarid2 knockdown reduced PRC2 at its target promoters, and ES cells devoid of the PRC2 component EED are deficient in Jarid2 promoter access. In addition to the well-documented defects in embryonic viability upon down-regulation of Jarid2, ES cell differentiation is impaired, as is Oct4 silencing. Examination of two factors in ES cells
2010-01-01 | E-GEOD-19708 | biostudies-arrayexpress
Project description:Polycomb repressive complex-2 (PRC2) is a group of proteins that play important role during development and in cell differentiation. PRC2 is a histone-modifying complex that catalyses methylation of lysine 27 of histone H3 (H3K27me3) at differentiation genes leading to their transcriptional repression. JARID2 is a co-factor of PRC2 and is important for targeting PRC2 to chromatin as well as modulating its activity. Here, we show that in many human cells, including human epidermal keratinocytes, JARID2 predominantly exists as a novel low molecular weight form, which lacks the N-terminal PRC2-interacting domain (ΔN-JARID2). We show that ΔN-JARID2 is a cleaved product of full-length JARID2 spanning the C-terminal conserved region consisting of jumonji domains. JARID2 knockout in keratinocytes results in up-regulation of cell cycle genes and repression of many epidermal differentiation genes. Surprisingly, repression of epidermal differentiation genes in JARID2-null keratinocytes can be relieved by expression of ΔN-JARID2 suggesting that this form promotes activation of these genes and has opposing function to that of PRC2 in regulation of differentiation. We propose that a switch from expression of full-length JARID2 to ΔN-JARID2 is important for the up-regulation of genes during differentiation.
2019-02-19 | GSE102116 | GEO
Project description:The Polycomb Group proteins foster gene repression profiles required for proper development and unimpaired adulthood, and comprise the components of the PRC2 complex including the histone H3 lysine 27 (H3K27) methyltransferase Ezh2. How mammalian PRC2 accesses chromatin is unclear. We find that Jarid2 associates with PRC2 and stimulates its enzymatic activity in vitro. Jarid2 contains a Jumonji C domain, but is devoid of detectable histone demethylase activity. Instead, its artificial recruitment to a promoter in vivo resulted in co-recruitment of PRC2 with resultant increased levels of H3K27me2/3. Jarid2 co-localizes with Ezh2 and MTF2, a homologue of Drosophila Pcl, at endogenous genes in ES cells. Jarid2 can itself bind DNA and its recruitment in ES cells is interdependent with that of PRC2 as Jarid2 knockdown reduced PRC2 at its target promoters, and ES cells devoid of the PRC2 component EED are deficient in Jarid2 promoter access. In addition to the well-documented defects in embryonic viability upon down-regulation of Jarid2, ES cell differentiation is impaired, as is Oct4 silencing.
2010-01-01 | GSE19708 | GEO
Project description:JARID2 ChIP-seq profile mediated by Xist was investigated using two separate approaches: In the first approach, we use the TX1072 female embryonic stem cell (ESC) line; this is a genetically polymorphic ESC line derived from a mouse with one X-chromosome (X-chr) from the Mus musculus castaneus (Cast) origin and the other of Mus musculus domesticus, C57BL/6 (BL6) strain origin, containing an inducible promoter on the BL6 Xist allele; differentiation and simultaneous induction of Xist for 4 days results in the inactivation of ONLY the BL6-derived X-chr and coating by JARID2 protein. We analysed this ESC line in the undifferentiated state, in which both X-chrs are active (and not coated by JARID2), and also after 4 days of differentiation under Xist inducible conditions, in which cells display one inactive X-chr from BL6 origin and one Xa of the Cast origin; the presence of SNPs allows for the comparison of the degree and localisation of JARID2 enrichment on the inactive X-chr versus the active X-chr; our results suggests that JARID2 is enriched on the inactive X-chr chromosome-wide and not in confined peaks as elsewhere in the genome; This pattern resembles patterns of Xist enrichment published before (Engreitz et al., 2013). In the second approach, we use a male ESC line that carries an inducible Xist transgene (TG) on chromosome 11 (chr11) (Wutz et al., 2000) in the presence (36:11 WT) or the absence of Eed (36:11 Eed-/-) Induction of Xist TG results in Xist coating and enrichment of JARID2 across the chr11, regardless of the presence of Eed when assess by IF/Xist RNA FISH experiments. We compare inducible and uninducible condition in both the 36:11 WT and Eed-/- ESCs; this way, we could assess the Xist-mediated JARID2 recruitment and the effect of the absence of Eed-/-; Our results shows that Xist induction result in a chromosome-wide enrichment of JARID2 on chr11, in a manner that resembles enrichment on the inactive X-chr; this pattern seem to be independent of EED, showing that in contrast to other regions in the genome where JARID2 occupancy is abrogated in the absence of EED, Xist-mediated JARID2 recruitment is not affected. JARID2 ChIP-seq analysis in differentiating female ESCs (TX1072) and in a male ESC harbouring a Xist transgene on chromosome 11 in WT and Eed-/- genetics settings
2014-01-23 | E-GEOD-52073 | biostudies-arrayexpress