PAR-CLIP for JARID2 before and after differentiation of mouse embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE60516 | GEO | 2014/08/20
SECONDARY ACCESSION(S): PRJNA258456
REPOSITORIES: GEO
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Project description:This experiment was designed to indentify RNAs making direct contact JARID2 as mouse ESCs differentiate E14 WT were left untreated or differentiated with 2 M-BM-5M RA for 24 hrs. In both cases, ceslls were pulsed with 4-SU, irradiated with UV, and subjected to JARID2 immunoprecipitation.
2014-08-20 | E-GEOD-60516 | biostudies-arrayexpress
Project description:This experiment was designed to identify RNAs making direct contact with JARID2 in mouse embryonic stem cells E14 cells were pulsed with 4-SU, irradiated with UV, and subjected to JARID2 immunoprecipitation.
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Project description:This experiment was designed to identify RNAs making direct contact with JARID2 in mouse embryonic stem cells
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2013-10-19 | GSE49433 | GEO
Project description:This experiment was designed to indentify RNAs making direct contact with EZH2 in mouse embryonic stem cells E14 with an integrated transgene encoding HA-EZH2 were pulsed with 4-SU, irradiated with UV, and subjected to HA immunoprecipitation.
2013-10-19 | E-GEOD-49433 | biostudies-arrayexpress
Project description:We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA.
2010-01-27 | GSE19365 | GEO
Project description:We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA. Examination of two different proteins in two different cell lines
2010-01-27 | E-GEOD-19365 | biostudies-arrayexpress
Project description:Somatic cell reprogramming can be achieved by cell fusion with embryonic stem cells (ESCs), nuclear transfer into oocytes, or forced expression of transcription factors essential for ESC identity. Reprogramming by transcription factors is a less efficient and slower process than that by other methods. Identification of a gene set capable of driving rapid and proper reprogramming to induced pluripotent stem cells (iPSCs) is an important issue. Here, we show that the efficiency and kinetics of iPSC reprogramming are dramatically improved by combined transduction of Jarid2, a gene highly expressed in both ESCs and oocytes and genes encoding its associated proteins. We demonstrate that forced expression of Jarid2 promotes iPSC reprogramming by suppressing the expression of Arf, a known reprogramming barrier, and that the N-terminal half of JARID2 is sufficient for such promotion. Moreover, Jarid2 accelerated retroviral transgene silencing and Nanog promoter demethylation, confirming its promoting activity. We further reveal that JARID2 physically interacts with ESRRB, SALL4A and PRDM14, and show that these JARID2-associated proteins synergistically and robustly facilitate iPSC reprogramming in a Jarid2-dependent manner. Our findings provide an insight into the important roles of Jarid2 during reprogramming, and suggest that the JARID2-associated protein network contributes to overcoming reprogramming barriers. We used microarrays to detect the up- and down-regulated genes in MEFs transduced with Jarid2 compared to empty vector control. Total RNA was extracted from mouse embrionc fibroblasts (MEFs) transduced with empty vector (control) or the indicated genes at 3 days post-transduction, and two iPSC clones from MEFs transduced with OSKM plus Jarid2. Gene expression profile was analyzed by the Affymetrix GeneChip microarray system.
2015-03-31 | E-GEOD-52200 | biostudies-arrayexpress
Project description:Somatic cell reprogramming can be achieved by cell fusion with embryonic stem cells (ESCs), nuclear transfer into oocytes, or forced expression of transcription factors essential for ESC identity. Reprogramming by transcription factors is a less efficient and slower process than that by other methods. Identification of a gene set capable of driving rapid and proper reprogramming to induced pluripotent stem cells (iPSCs) is an important issue. Here, we show that the efficiency and kinetics of iPSC reprogramming are dramatically improved by combined transduction of Jarid2, a gene highly expressed in both ESCs and oocytes and genes encoding its associated proteins. We demonstrate that forced expression of Jarid2 promotes iPSC reprogramming by suppressing the expression of Arf, a known reprogramming barrier, and that the N-terminal half of JARID2 is sufficient for such promotion. Moreover, Jarid2 accelerated retroviral transgene silencing and Nanog promoter demethylation, confirming its promoting activity. We further reveal that JARID2 physically interacts with ESRRB, SALL4A and PRDM14, and show that these JARID2-associated proteins synergistically and robustly facilitate iPSC reprogramming in a Jarid2-dependent manner. Our findings provide an insight into the important roles of Jarid2 during reprogramming, and suggest that the JARID2-associated protein network contributes to overcoming reprogramming barriers. We used microarrays to detect the up- and down-regulated genes in MEFs transduced with Jarid2 compared to empty vector control.
2015-03-31 | GSE52200 | 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