Cardiac-specific developmental and epigenetic functions of Jarid2 during embryonic development
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PROVIDER: PRJNA454380 | ENA |
REPOSITORIES: ENA
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Project description:Jarid2 cooperates with PRC2 for H3K27me3 accumulation on a subset of Jarid2 target genes in the developing heart, which contributes to repress differentiation of other lineages such as neural differentiation, and to guide normal myocardial development. Jarid2 forms a functional complex with PRC2 to increase or maintain H3K27me3 levels on the specific promoters in the developing heart.
2018-05-02 | GSE113895 | GEO
Project description:Epigenetic regulation is critical in normal cardiac development. We have demonstrated that the deletion of Jarid2 (Jumonji (Jmj) A/T-rich interaction domain 2) in mice results in cardiac malformations recapitulating human congenital cardiac disease and dysregulation of gene expression. However, the precise developmental and epigenetic functions of Jarid2 within the developing heart remain to be elucidated. Here, we determined the cardiac-specific functions of Jarid2 and the genetic networks regulated by Jarid2. Jarid2 was deleted using different cardiac-specific Cre mice. The deletion of Jarid2 by Nkx2.5-Cre mice (Jarid2Nkx) caused cardiac malformations including ventricular septal defects, thin myocardium, hypertrabeculation, and neonatal lethality. Jarid2Nkx mice exhibited elevated expression of neural genes, cardiac jelly, and other key factors including Isl1 and Bmp10 in the developing heart. By employing combinatorial genome-wide approaches and molecular analyses, we showed that Jarid2 in the myocardium regulates a subset of Jarid2 target gene expression and H3K27me3 enrichment during heart development. Specifically, Jarid2 was required for PRC2 occupancy and H3K27me3 at the Isl1 promoter locus, leading to the proper repression of Isl1 expression. In contrast, Jarid2 deletion in differentiated cardiomyocytes by cTnt-Cre mice caused no gross morphological defects or neonatal lethality. Thus, the early deletion of Jarid2 in cardiac progenitors, prior to the differentiation of cardiac progenitors into cardiomyocytes, results in morphogenetic defects manifested later in development. Our studies reveal that there is a critical window during early cardiac progenitor differentiation when Jarid2 is crucial to establish the epigenetic landscape at later stages of development.
| S-EPMC6066322 | biostudies-literature
Project description:Jarid2, a member of the Jumanji family of proteins, is a developmental regulator that is necessary for proper mouse development and stem cell differentiation. To investigate the specific functions of Jarid2 during pancreas development, we generated pancreas-specific Jarid2 mutants. We used microarrays to determine gene expression changes resulting from deletion of the Jarid2 gene in the pancreas.
2017-09-26 | GSE77238 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE33546: Polycomb repressive complex 2-dependent and M-bM-^@M-^Sindependent functions of Jarid2 in transcriptional regulation in Drosophila [ChIP-Seq] GSE36038: Polycomb repressive complex 2-dependent and M-bM-^@M-^Sindependent functions of Jarid2 in transcriptional regulation in Drosophila [Affymetrix] Refer to individual Series
2012-02-23 | E-GEOD-36039 | biostudies-arrayexpress
Project description:Jarid2 was recently identified as an important component of the mammalian Polycomb Repressive Complex 2 (PRC2), where it has a major effect on PRC2 recruitment in mouse embryonic stem cells. Although Jarid2 is conserved in Drosophila, it has not previously been implicated in Polycomb (Pc) regulation. Therefore, we purified Drosophila Jarid2 and its associated proteins and find that Jarid2 associates with all of the known canonical PRC2 components, demonstrating a conserved physical interaction with PRC2 in flies and mammals. Furthermore, in vivo studies with Jarid2 mutants in flies demonstrate that among several histone modifications tested, only H3K27 methylation, the mark implemented by PRC2, was affected. Genome-wide profiling of Jarid2, Su(z)12 and H3K27me3 occupancy by ChIP-seq indicates that Jarid2 and Su(z)12 have a very similar distribution pattern on chromatin. However, Jarid2 and Su(z)12 occupancy levels at some genes are significantly different with Jarid2 being present at relatively low levels at many Pc response elements (PREs) of certain Homeobox (Hox) genes, providing a rationale for why Jarid2 was never identified in Pc screens. Gene expression analyses show that Jarid2 and E(z) (a canonical PRC2 component) are required not only for transcriptional repression but might also function in active transcription. Identification of Jarid2 as a conserved PRC2 interactor in flies provides an opportunity to begin to probe some of its novel functions in Drosophila development. Examination of Jarid2, Su(z)12, and H3K27me3 profiles in fly larvae and Su(z)12 in eye imaginal discs under wild-type and Jarid2 mutant conditions.
2012-02-23 | E-GEOD-33546 | biostudies-arrayexpress
Project description:Jarid2 was recently identified as an important component of the mammalian Polycomb Repressive Complex 2 (PRC2), where it has a major effect on PRC2 recruitment in mouse embryonic stem cells. Although Jarid2 is conserved in Drosophila, it has not previously been implicated in Polycomb (Pc) regulation. Therefore, we purified Drosophila Jarid2 and its associated proteins and find that Jarid2 associates with all of the known canonical PRC2 components, demonstrating a conserved physical interaction with PRC2 in flies and mammals. Furthermore, in vivo studies with Jarid2 mutants in flies demonstrate that among several histone modifications tested, only H3K27 methylation, the mark implemented by PRC2, was affected. Genome-wide profiling of Jarid2, Su(z)12 and H3K27me3 occupancy by ChIP-seq indicates that Jarid2 and Su(z)12 have a very similar distribution pattern on chromatin. However, Jarid2 and Su(z)12 occupancy levels at some genes are significantly different with Jarid2 being present at relatively low levels at many Pc response elements (PREs) of certain Homeobox (Hox) genes, providing a rationale for why Jarid2 was never identified in Pc screens. Gene expression analyses show that Jarid2 and E(z) (a canonical PRC2 component) are required not only for transcriptional repression but might also function in active transcription. Identification of Jarid2 as a conserved PRC2 interactor in flies provides an opportunity to begin to probe some of its novel functions in Drosophila development. Expression analyses of Jarid2 mutants in larvae and eye imaginal discs. Expression analyses of E(z) RNAi in larvae.
2012-02-23 | E-GEOD-36038 | biostudies-arrayexpress
Project description:Jarid2 was recently identified as an important component of the mammalian Polycomb Repressive Complex 2 (PRC2), where it has a major effect on PRC2 recruitment in mouse embryonic stem cells. Although Jarid2 is conserved in Drosophila, it has not previously been implicated in Polycomb (Pc) regulation. Therefore, we purified Drosophila Jarid2 and its associated proteins and find that Jarid2 associates with all of the known canonical PRC2 components, demonstrating a conserved physical interaction with PRC2 in flies and mammals. Furthermore, in vivo studies with Jarid2 mutants in flies demonstrate that among several histone modifications tested, only H3K27 methylation, the mark implemented by PRC2, was affected. Genome-wide profiling of Jarid2, Su(z)12 and H3K27me3 occupancy by ChIP-seq indicates that Jarid2 and Su(z)12 have a very similar distribution pattern on chromatin. However, Jarid2 and Su(z)12 occupancy levels at some genes are significantly different with Jarid2 being present at relatively low levels at many Pc response elements (PREs) of certain Homeobox (Hox) genes, providing a rationale for why Jarid2 was never identified in Pc screens. Gene expression analyses show that Jarid2 and E(z) (a canonical PRC2 component) are required not only for transcriptional repression but might also function in active transcription. Identification of Jarid2 as a conserved PRC2 interactor in flies provides an opportunity to begin to probe some of its novel functions in Drosophila development.
2012-02-23 | GSE36038 | GEO
Project description:Jarid2 was recently identified as an important component of the mammalian Polycomb Repressive Complex 2 (PRC2), where it has a major effect on PRC2 recruitment in mouse embryonic stem cells. Although Jarid2 is conserved in Drosophila, it has not previously been implicated in Polycomb (Pc) regulation. Therefore, we purified Drosophila Jarid2 and its associated proteins and find that Jarid2 associates with all of the known canonical PRC2 components, demonstrating a conserved physical interaction with PRC2 in flies and mammals. Furthermore, in vivo studies with Jarid2 mutants in flies demonstrate that among several histone modifications tested, only H3K27 methylation, the mark implemented by PRC2, was affected. Genome-wide profiling of Jarid2, Su(z)12 and H3K27me3 occupancy by ChIP-seq indicates that Jarid2 and Su(z)12 have a very similar distribution pattern on chromatin. However, Jarid2 and Su(z)12 occupancy levels at some genes are significantly different with Jarid2 being present at relatively low levels at many Pc response elements (PREs) of certain Homeobox (Hox) genes, providing a rationale for why Jarid2 was never identified in Pc screens. Gene expression analyses show that Jarid2 and E(z) (a canonical PRC2 component) are required not only for transcriptional repression but might also function in active transcription. Identification of Jarid2 as a conserved PRC2 interactor in flies provides an opportunity to begin to probe some of its novel functions in Drosophila development.
2012-02-23 | GSE33546 | GEO
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.
2013-12-25 | E-GEOD-48517 | biostudies-arrayexpress
Project description:Analysis of the binding of Jarid2 in mouse ES cells using a Flag tagged version of Jarid2 and a anti-Flag antibody.
2010-04-13 | E-TABM-963 | biostudies-arrayexpress