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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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. 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).

ORGANISM(S): Homo sapiens

SUBMITTER: Agustin Chicas

PROVIDER: E-GEOD-43920 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Chicas Agustin A Kapoor Avnish A Wang Xiaowo X Aksoy Ozlem O Evertts Adam G AG Zhang Michael Q MQ Garcia Benjamin A BA Bernstein Emily E Lowe Scott W SW

Proceedings of the National Academy of Sciences of the United States of America 20120521 23

Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. Here we combine quantitative mass spectrometry, ChIP deep-sequencing, and functional studies to determine the role of histone modifications on chromatin structure and gene-expression alterations associated with senescence in primary human cells. We uncover distinct senescence-associated changes in histone-modification pa ...[more]

PMID: 22615382

Similar Datasets

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.

2013-01-31 | GSE43920 | 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

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. Compare gene expression of Jarid1B Knock Out and Wild type Mammary Epithelial Cells (MECs).

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

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

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. Examination of Jarid1b and H3K4me3 in mouse ES cells

2011-10-26 | E-GEOD-31966 | 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

miR-34 regulates JARID1A expresion (NB1691)

Project description:p53 inactivation occurs only rarely in neuroblastoma, although miR-34, a transcriptional target of p53, is often deleted in neuroblastoma, suggesting another way in which p53 signaling might be impaired. In this study we show that miR-34 directly targets and downregulates the Polycomb Repressive Complex 2 (PRC2) and its associated histone demethylase, JARID1A, in a p53-dependent manner, 8 samples were transfected with siRNA control or JMJD2B, MYCN, JARID1A into NB1691 cells.

2014-01-01 | E-GEOD-49854 | 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

Expression data from either growing IMR90 human fibroblasts or senescent IMR90 cells with Ras expression and indicated hairpins

Project description:Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes. To understand the contribution of different genes, especially E2F7 to the expression profile of senescent cells, we infected human IMR90 cells with Ras and different hairpins. The infected population was selected using first with 2 ug/ml puromycin (Sigma) for 2 days, then 100 ug/ml hygromycin B (Roche) for 3 days. RNA was isolated 7 days after the puromycin selection and hybridized to Affymetrix microarrays. We tried to understand the effect of E2F7 in the transcription profile of senescent cells.

2012-08-25 | E-GEOD-40349 | biostudies-arrayexpress

Transcription profiling of human IMR90 cells after RNAi suppression of RB, p107 or p130 using in growing, quiescent or ras-induced senescent IMR90 cells

Project description:The action of RB as a tumor suppressor has been difficult to define, in part, due to the redundancy of the related proteins p107 and p130. By coupling advanced RNAi technology to suppress RB, p107 or p130 with a genome wide analysis of gene expression in growing, quiescent or ras-senescent cells, we identified a unique and specific activity of RB in repressing DNA replication as cells exit the cell cycle into senescence, a tumor suppressive program. Experiment Overall Design: Expression profiles of IMR90 cells before and after RNAi-mediated supppression of RB, p107 or p130 in growing, quiescent or ras-induced senescent conditions. RNA was extracted from growing, low serum (0.1% FBS), confluent, or ras-senescent cells.

2010-01-23 | E-GEOD-19864 | biostudies-arrayexpress

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