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Jarid1b targets genes regulating development and is involved in neural differentiation [expression array]

ABSTRACT: The H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) is dispensable for embryonic stem cell (ESC) self-renewal, but essential for ESC differentiation along the neural lineage. During neural differentiation, Jarid1b depleted ESCs fail to efficiently silence lineage-inappropriate genes, specifically stem and germ cell genes. Our results delineate an essential role for Jarid1b-mediated transcriptional control during ESC differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE31967 | GEO | 2011/10/27

SECONDARY ACCESSION(S): PRJNA155271

REPOSITORIES: GEO

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Jarid1b targets genes regulating development and is involved in neural differentiation [expression array]

Project description:The H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) is dispensable for embryonic stem cell (ESC) self-renewal, but essential for ESC differentiation along the neural lineage. During neural differentiation, Jarid1b depleted ESCs fail to efficiently silence lineage-inappropriate genes, specifically stem and germ cell genes. Our results delineate an essential role for Jarid1b-mediated transcriptional control during ESC differentiation. Control (LKOScr) or Jarid1b knockdown (LKOJarid1b) mouse ES cells were used.Each experiment was performed in triplicates.

2011-10-26 | E-GEOD-31967 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3 [ChIP-Seq]

Project description:Embryonic development is tightly regulated by transcription factors and chromatin-associated proteins. H3K4me3 is associated with active transcription and H3K27me3 with gene repression, while the combination of both keeps genes required for development in a plastic state. Here we show that deletion of the H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) results in major neonatal lethality due to respiratory failure. Jarid1b knockout embryos have several neural defects including disorganized cranial nerves, defects in eye development and increased incidences of exencephaly. Moreover, in line with an overlap of Jarid1b and Polycomb targets genes, Jarid1b knockout embryos display homeotic skeletal transformations typical for Polycomb mutants. Genome-wide analysis demonstrated that normally inactive genes encoding developmental regulators acquire aberrant H3K4me3 in early Jarid1b knockout embryos. H3K4me3 accumulates as embryonic development proceeds, leading to increased expression of neural master regulators in knockouts. Taken together, these results suggest that Jarid1b contributes to mouse development by protecting developmental genes from inappropriate acquisition of active histone modifications. * Lack of Jarid1b leads to major neonatal lethality and defects in neural systems * Jarid1b mutants display homeotic skeletal transformations * H3K4me3 is increased at inactive transcriptional regulators in Jarid1b-/- embryos * Chromatin changes are accompanied by elevated levels of key neural transcription factors Determining H3K4me3 and H3K27me3 in early (E8.5) mouse embryos

2013-04-26 | E-GEOD-41172 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3 [Affymetrix]

Project description:Embryonic development is tightly regulated by transcription factors and chromatin-associated proteins. H3K4me3 is associated with active transcription and H3K27me3 with gene repression, while the combination of both keeps genes required for development in a plastic state. Here we show that deletion of the H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) results in major neonatal lethality due to respiratory failure. Jarid1b knockout embryos have several neural defects including disorganized cranial nerves, defects in eye development and increased incidences of exencephaly. Moreover, in line with an overlap of Jarid1b and Polycomb targets genes, Jarid1b knockout embryos display homeotic skeletal transformations typical for Polycomb mutants. Genome-wide analysis demonstrated that normally inactive genes encoding developmental regulators acquire aberrant H3K4me3 in early Jarid1b knockout embryos. H3K4me3 accumulates as embryonic development proceeds, leading to increased expression of neural master regulators in knockouts. Taken together, these results suggest that Jarid1b contributes to mouse development by protecting developmental genes from inappropriate acquisition of active histone modifications. * Lack of Jarid1b leads to major neonatal lethality and defects in neural systems * Jarid1b mutants display homeotic skeletal transformations * H3K4me3 is increased at inactive transcriptional regulators in Jarid1b-/- embryos * Chromatin changes are accompanied by elevated levels of key neural transcription factors RNA was extracted from heads of E8.5 embryos, three pools of 4 heads each were used per genotype

2013-04-26 | E-GEOD-41171 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3 [Affymetrix]

2013-04-26 | GSE41171 | GEO

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3 [ChIP-Seq]

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Histone Demethylase JARID1B Controls Mammary Gland Development by Regulating Key Developmental Genes

Project description:The jmjC-domain containing H3K4 histone demethylase JARID1B/KDM5B/PLU1 is over-expressed in human breast cancer and is a potential target for breast cancer treatment. To investigate the in vivo function of JARID1B, we developed a new strain of Jarid1b knockout mice and characterized the phenotypes in detail. Unlike previously reported knockout strains, the majority of our Jarid1b knockout mice are viable beyond embryonic and neonatal stages. Nonetheless, these mice exhibit decreased body weight, higher incidence of adult mortality and decreased female fertility. Furthermore, Jarid1b knockout mice show delayed mammary gland development. Mechanistically, loss of JARID1B leads to decreased serum estrogen levels and reduced proliferation of mammary epithelial cells in early puberty. In addition, in mammary epithelial cells, loss of JARID1B diminishes the expression of key regulators of mammary morphogenesis, including FOXA1, estrogen receptor α (ERα), and GATA3. Taken together, these results indicate that JARID1B positively regulates mammary ductal development through both extrinsic and cell-autonomous mechanisms.

2014-05-19 | GSE50479 | GEO

Histone Demethylase JARID1B Controls Mammary Gland Development by Regulating Key Developmental Genes

2014-05-19 | E-GEOD-50479 | biostudies-arrayexpress

Jarid1b targets genes regulating development and is involved in neural differentiation

Project description:This SuperSeries is composed of the following subset Series: GSE31966: Jarid1b targets genes regulating development and is involved in neural differentiation [ChIP-seq] GSE31967: Jarid1b targets genes regulating development and is involved in neural differentiation [expression array] Refer to individual Series

2011-10-26 | E-GEOD-31968 | biostudies-arrayexpress

Jarid1b targets genes regulating development and is involved in neural differentiation [ChIP-seq]

Project description:We analyzed the genome-wide binding profile of Jarid1b in mouse ESCs. We find that Jarid1b localizes mainly to transcription start sites, of which more than 50% are also bound by Polycomb proteins and are enriched for genes encoding developmental regulators. Furthermore, we generated genome-wide mapping of H3K4me3 in LKO Scramble and LKO Jarid1b mouse ESCs. Virtually all Jarid1b binding sites are positive for H3K4me3. Upon knockdown of Jarid1b, H3K4me3 is significantly increased at Jarid1b positive regions.

2011-10-27 | GSE31966 | GEO

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Project description:Genome-wide maps of KDM5A/JARID1A/RBP2 and KDM5B/JARID1B/PLU1 in estrogen treated MCF7 cells.

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