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H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence (expression)

ABSTRACT: Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We have examined the effect of suppressing the histone demethylases Jarid1a and Jarid1b on the senescence-associated gene expression signatures.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43920 | GEO | 2013/01/31

SECONDARY ACCESSION(S): PRJNA188185

REPOSITORIES: GEO

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H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence (expression)

Project description:Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We have examined the effect of suppressing the histone demethylases Jarid1a and Jarid1b on the senescence-associated gene expression signatures. Human fibroblast (IMR90) cells were infected with retroviral vectors expresssing shRNA targeting Jarid1a, Jarid1b or both, and triggered to undergo quiescence by removal of serum or senescence by over-expression of activated ras (Hrasv12).

2013-01-31 | E-GEOD-43920 | biostudies-arrayexpress

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence (ChIP-seq)

2013-01-31 | GSE43921 | GEO

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence (ChIP-seq)

Project description:Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We combined quantitative mass spectrometry and ChIP deep-sequencing to identify changes in histone modification occurring during cellular senescence. ChIP-seq was carried out using H3K4me3-specific antibodies in growing, quiescent, senescent, or senescent with shRB targeting Rb, IMR90 cells. The control mock data (ChIP-seq using anti-mouse IgG antibody) is available in GEO Sample GSM497500 (Series GSE19898).

2013-01-31 | E-GEOD-43921 | biostudies-arrayexpress

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence.

Project description: Not available

| S-EPMC3384172 | biostudies-literature

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-01-31 | GSE43922 | GEO

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-31 | E-GEOD-43922 | biostudies-arrayexpress

Physical and functional interactions between the histone H3K4 demethylase JARID1A and the NuRD complex

Project description:Histone H3K4 methylation has been linked to transcriptional activation. JARID1A (also known as RBP2 or KDM5A), a member of the JARID1 protein family, is an H3K4 demethylase, previously implicated in the regulation of transcription and differentiation. Here we show that JARID1A is physically and functionally associated with two histone deacetylase complexes. Immunoaffinity purification of JARID1A confirmed a previously described association with the SIN3B-containing HDAC complex, and revealed an association with the nucleosome remodeling and deacetylase (NuRD) complex. Sucrose density gradient and sequential immunoprecipitation analyses further confirmed the stable association of JARID1A with these two HDAC complexes. JARID1A depletion led to changes in the expression of hundreds of genes, two-thirds of which were also controlled by CHD4, the NuRD catalytic subunit. Gene ontology analysis confirmed that the genes commonly regulated by both JARID1A and CHD4 were categorized as developmentally regulated genes. ChIP analyses suggested that CHD4 controls chromatin association with JARID1A and modulates H3K4 levels at the promoter and coding regions of target genes. We further demonstrated that the C. elegans homologues of JARID1 and CHD4 function in the same pathway during vulva development. Taken together, these results suggest that JARID1A and the NuRD complex cooperatively function to control developmentally regulated genes.

2014-02-21 | GSE55206 | GEO

Physical and functional interactions between the histone H3K4 demethylase JARID1A and the NuRD complex

2014-02-21 | E-GEOD-55206 | 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

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

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