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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The DAXX co-repressor is directly recruited to active regulatory elements genome-wide to regulate autophagy programs in a model of human prostate cancer

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

ORGANISM(S): Homo sapiens

SUBMITTER: Christopher Benner

PROVIDER: E-GEOD-68656 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The DAXX co-repressor is directly recruited to active regulatory elements genome-wide to regulate autophagy programs in a model of human prostate cancer.

Puto Lorena A LA Benner Christopher C Hunter Tony T

Oncoscience 20150417 4

While carcinoma of the prostate is the second most common cause of cancer death in the US, current methods and markers used to predict prostate cancer (PCa) outcome are inadequate. This study was aimed at understanding the genome-wide binding and regulatory role of the DAXX transcriptional repressor, recently implicated in PCa. ChIP-Seq analysis of genome-wide distribution of DAXX in PC3 cells revealed over 59,000 DAXX binding sites, found at regulatory enhancers and promoters. ChIP-Seq analysis ...[more]

PMID: 26097870

Similar Datasets

The DAXX co-repressor is directly recruited to active regulatory elements genome-wide to regulate autophagy programs in a model of human prostate cancer (ChIP-seq)

Project description:This study was aimed at understanding the genome-wide binding and regulatory role of the DAXX transcriptional repressor, recently implicated in PCa. ChIP-Seq analysis of genome-wide distribution of DAXX in PC3 cells revealed over 59,000 DAXX binding sites, found at regulatory enhancers and promoters. ChIP-Seq analysis of DNA methyltransferase 1 (DNMT1), which is a key epigenetic partner for DAXX repression, revealed that DNMT1 binding was restricted to a small number of DAXX sites. DNMT1 and DAXX bound close to transcriptional activator motifs. DNMT1 sites were found to be dependent on DAXX for recruitment by analyzing DNMT1 ChIP-Seq following DAXX knockdown (K/D), corroborating previous findings that DAXX recruits DNMT1 to repress its target genes. Massively parallel RNA sequencing (RNA-Seq) was used to compare the transcriptomes of WT and DAXX K/D PC3 cells. Genes induced by DAXX K/D included those involved in autophagy, and DAXX ChIP-Seq peaks were found close to the transcription start sites (TSS) of autophagy genes, implying they are more likely to be regulated by DAXX. To determine DAXX binding sites in the prostate cancer (PCa) genome, the PC3 cell line was used. A stable DAXX shRNA knockdown (K/D) PC3 cell line and a control shRNA counterpart, were compared in a ChIP-Seq study.

2015-06-24 | E-GEOD-68647 | biostudies-arrayexpress

The DAXX co-repressor is directly recruited to active regulatory elements genome-wide to regulate autophagy programs in a model of human prostate cancer (RNA-seq)

Project description:This study was aimed at understanding the genome-wide binding and regulatory role of the DAXX transcriptional repressor, recently implicated in PCa. ChIP-Seq analysis of genome-wide distribution of DAXX in PC3 cells revealed over 59,000 DAXX binding sites, found at regulatory enhancers and promoters. ChIP-Seq analysis of DNA methyltransferase 1 (DNMT1), which is a key epigenetic partner for DAXX repression, revealed that DNMT1 binding was restricted to a small number of DAXX sites. DNMT1 and DAXX bound close to transcriptional activator motifs. DNMT1 sites were found to be dependent on DAXX for recruitment by analyzing DNMT1 ChIP-Seq following DAXX knockdown (K/D), corroborating previous findings that DAXX recruits DNMT1 to repress its target genes. Massively parallel RNA sequencing (RNA-Seq) was used to compare the transcriptomes of WT and DAXX K/D PC3 cells. Genes induced by DAXX K/D included those involved in autophagy, and DAXX ChIP-Seq peaks were found close to the transcription start sites (TSS) of autophagy genes, implying they are more likely to be regulated by DAXX. Determine changes in gene expression levels between WT and DAXX K/D prostate cancer cells by RNA-Seq (PC3 Cells).

2015-06-24 | E-GEOD-68645 | biostudies-arrayexpress

Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets

2015-06-08 | E-GEOD-66899 | biostudies-arrayexpress

Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

Project description:The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed. ChIP-seq was performed for Blimp-1-eGFP in duplicate in E18.5 small intestine expressing the fusion protein using anti-GFP antibody. As a negative control a single anti-GFP ChIP was also performed in wild type small intestine. ChIP-seq for Irf-1 was performed in duplicate in both wild type and Prdm1/Blimp-1 mutant E18.5 small intestine using an anti-Irf-1 antibody. Duplicate IgG ChIP control in wild types was performed as a negative control. All samples had an associated input chromatin sample sequenced.

2015-07-10 | E-GEOD-66069 | biostudies-arrayexpress

The Mediator complex subunit MED23 couples H2B mono-ubiquitination to transcriptional control and cell fate determination

Project description:The Mediator complex orchestrates multiple transcription factors with the Pol II apparatus for precise transcriptional control. However, its interplay with the surrounding chromatin remains poorly understood. Here, we analyze differential histone modifications between WT and MED23-/- (KO) cells and identify H2B mono-ubiquitination at lysine 120 (H2Bub) as a MED23-dependent histone modification. Using tandem affinity purification and mass spectrometry, we find that MED23 associates with the RNF20/40 complex, the enzyme for H2Bub, and show that this association is critical for the recruitment of RNF20/40 to chromatin. In a cell-free system, Mediator directly and substantially increases H2Bub on recombinant chromatin through its cooperation with RNF20/40 and the PAF complex. Integrative genome-wide analyses show that MED23 depletion specifically reduces H2Bub on a subset of MED23-contolled genes. Importantly, MED23-coupled H2Bub levels are oppositely regulated during myogenesis and lung carcinogenesis. In sum, these results establish a mechanistic link between the Mediator complex and a critical chromatin modification in coordinating transcription with cell growth and differentiation. To examine the enrichment of H2B ubiquitination, Pol II, H3K4me3, H3K79me3 in WT and KO MED23 MEF cells, we performed H2Bub ChIP-seq, Pol II ChIP-seq, H3K4me3 ChIP-seq and H3K79me3 ChIP-seq assays. 10 high-throughput sequencing data were deposited and WT, KO input data were controls for peak calling.

2015-09-16 | E-GEOD-59518 | biostudies-arrayexpress

Essential control of early B-cell development by Mef2 transcription factors

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

2015-12-14 | E-GEOD-73563 | biostudies-arrayexpress

The PR/SET domain Zinc finger protein Prdm4 regulates gene expression in ES cells but plays a non-essential role in the developing mouse embryo.

Project description:ChIP-seq using anti-GFP antibody to map genomic binding of Prdm4-EGFP in stably transfected mouse embryonic stem cells Two independent ChIP-seq replicates for each of two independent Prdm4-EGFP expressing ES cell clones resulting in four anti-GFP ChIP-seq experiments. These samples have paired mouse IgG control.

2013-08-08 | E-GEOD-48372 | biostudies-arrayexpress

ChIP-seq of neuroblastoma IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5 cell lines to identify TBX2, MYCN, H3K27ac, H3K4me1 and H3K4me3 binding sites

Project description:ChIP-seq to define bindings sites for TBX2, MYCN, H3K27ac, H3K4me1, H3K4me3 and Input in the cell lines IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5.

2018-10-16 | E-MTAB-6570 | biostudies-arrayexpress

The nuclear receptor ERbeta engages AGO2 in regulation of gene transcription, RNA splicing and RISC loading. Part 5

Project description:The RNA-binding protein Argonaute 2 (AGO2) is a key effector of RNA-silencing pathways It exerts a pivotal role in microRNA maturation and activity, and can modulate chromatin remodeling, transcriptional gene regulation and RNA splicing. The Estrogen Receptor beta (ERβ) is endowed with oncosuppressive activities, antagonizing hormone-induced carcinogenesis and inhibiting growth and oncogenic functions in luminal-like breast cancers (BCs), where its expression correlates with a better prognosis of the disease. Applying interaction proteomics coupled to mass spectrometry (MS) to characterize nuclear factors cooperating with ERβ in gene regulation, we identify AGO2 as a novel partner of ERβ in human BC cells. ERβ-AGO2 association was confirmed in vitro and in vivo both in the nucleus and in cytoplasm and is shown to be RNA-mediated. ChIP-Seq demonstrates AGO2 association to a large number of ERβ binding sites, and total and nascent RNA-Seq in ERβ+ vs ERβ- cells, and before and after AGO2 knock-down in ERβ+ cells, reveals a widespread involvement of this factor in ERβ-mediated regulation of gene transcription rate and RNA splicing. Moreover, isolation and sequencing by RIP-Seq of ERβ-associated long and small RNAs in the cytoplasm suggests involvement of the nuclear receptor in RISC loading, indicating that it may able to control directly also mRNA translation efficiency and stability.These results demonstrate that AGO2 can act as a pleiotropic functional partner of ERβ, indicating that both factors are endowed with multiple roles in the control of key cellular functions

2017-04-25 | E-MTAB-4359 | biostudies-arrayexpress

P300 ChIP-Seq analysis of PC3 cells treated with MnTE-2-PyP or not 24 hours prior to irradiation of 20 Gy.

Project description:In order to identify how MnTE-2-PyP affects p300 association to chromatin genome-wide, we performed a p300 chromatin Immunoprecipitation assay followed by Next Generation Sequencing on PC3 cells treated with or without MnTE-2-PyP one hour post-irradiation (Figure 3A). Based on the called peaks near genes, we predicted that HIF-1Î²and CREB transcription factors were associating DNA less in the presence of MnTE-2-PyP. DNA was ChIP-Fixed from Pc3 cells treated with 20 Gy radiation and with and without T2E drug. There are 2 biological replicates of PC3 untreated cells and 3 biological replicates of PC3 cells treated with MnTE-2-PyP. There are two corresponding input samples for the biological replicates.

2015-10-27 | E-GEOD-74351 | biostudies-arrayexpress

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