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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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NO001: Kdm5c controls promoter and enhancer activities

ABSTRACT: RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells

ORGANISM(S): Mus musculus

SUBMITTER: Marian Groot Koerkamp

PROVIDER: E-MTAB-1177 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Balancing of histone H3K4 methylation states by the Kdm5c/SMCX histone demethylase modulates promoter and enhancer function.

Outchkourov Nikolay S NS Muiño Jose M JM Kaufmann Kerstin K van Ijcken Wilfred F J WF Groot Koerkamp Marian J MJ van Leenen Dik D de Graaf Petra P Holstege Frank C P FC Grosveld Frank G FG Timmers H T Marc HT

Cell reports 20130328 4

The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes such as enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in mouse embryonic ...[more]

PMID: 23545502

Similar Datasets

NO001: Kdm5c controls promoter and enhancer activities

Project description:The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes like enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in embryonic stem cells and neuronal progenitor cells via gene-specific transcription factors. Knockdown of Kdm5c deregulates transcription via local increases in H3K4me3. Our data show that restricting H3K4me3 modification at core promoters dampens transcription, but Kdm5c is required at enhancers for their full activity. Remarkably, an impaired enhancer function activates the intrinsic promoter activity of Kdm5c-bound distal elements. Our results demonstrate that the Kdm5c demethylase plays a crucial and dynamic role in the functional discrimination between enhancers and core promoters. RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells.

2013-04-05 | E-GEOD-38862 | biostudies-arrayexpress

The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

2013-04-01 | E-GEOD-34975 | biostudies-arrayexpress

scGET-seq profile of NIH-3T3 cells with Kdm5c knockdown

Project description:scGET-seq profiling of NIH3T3 cells in which Kdm5c was silenced with antisense shRNA or with a control scramble shRNA.

2021-08-17 | E-MTAB-9651 | biostudies-arrayexpress

KDM5C safeguards the appropriate timing of early neurodevelopment

Project description:We generated human induced pluripotent cells from intellectual disability patients carrying the c.2T>C mutation in KDM5C (Called “Mutant”). We generated a paired, isogenic human iPS cell line (called “Corrected”) using CRISPR/Cas9 and PiggyBac gene-editing technologies and conducted neuronal differentiation based on “Yichen Shi et al. Nat. Protoc. 7, 1836–1846 (2012)” to define differences in gene expression between the Mutant and Corrected during neurodevelopment.

2023-10-13 | E-MTAB-7551 | biostudies-arrayexpress

RNA-seq of SH-SY5Y NB cells stably transduced with shETV5 compared to parental cells, cell line samples and samples of xenografted tumors

Project description:Stable ETV5 knockdown SH-SY5Y were used to investigate the role of ETV5 in vitro and in vivo. Libraries for mRNA sequencing were prepared using the TruSeq stranded mRNA sample prep kit (Illumina), involving polyA-selection, fragmentation, adapter ligation, reverse transcription and PCR amplification. Libraries were quantified using the Qubit 2.0 Fluorometer prior to sequencing with read length of 75 bp on a NextSeq 500 sequencer (Illumina). On average 24.7 M high-quality reads were generated per sample, with a minimal read count of 20.0 M reads for sample 2015_027_009 (sample L105). For each sample, gene-level read counts and KPKM-values were generated with Sailfish (Patro et al. 2014). Read counts are the number of reads overlapping a given feature such as a gene. KPKM-values (K-mers Per Kilobase of exon per Million reads) represent read counts normalized for sequencing depth and transcript length. KPKM-values allow you to compare genes across and within samples.

2020-05-01 | E-MTAB-6713 | biostudies-arrayexpress

Transcription profiling by array of Fanconi Anemia patient (FANCA) EBV cell line transduced with control shRNA or a shRNA targeting p53 and treated with a Mitomycin C (MMC) pulse

Project description:Time point (H0, H24, H72) expression data from an EBV cell line obtained from a Fanconi Anemia patient (FANCA) transduced with a control shRNA (sh Ctrl) (n=3) or a shRNA targeting p53 (sh p53) (n=3) and treated with a brief MMC pulse.

2012-10-23 | E-MTAB-1099 | biostudies-arrayexpress

In vivo NCL-targeting affects breast cancer aggressiveness through miRNA regulation [RNA-seq]

Project description:Numerous studies have described the altered expression and the causal role of miRNAs in human cancer. However, to date efforts to modulate miRNA levels for therapeutic purposes have been challenging to implement. Here, we find that Nucleolin (NCL), a major nucleolar protein, post-transcriptionally regulates the expression of a specific subset of miRNAs, including miR-21, miR-221, miR-222, and miR-103, causally involved in breast cancer initiation, progression and drug-resistance. We also show that NCL is commonly overexpressed in human breast tumors, and its expression correlates with that of NCL-dependent miRNAs. Finally, this study indicates that NCL-binding guanosine-rich aptamers affect the levels of NCL-dependent miRNAs and their target genes, reducing breast cancer cell aggressiveness, both in vitro and in vivo. These findings illuminate a path to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expression in the treatment of breast cancer. Identification of NCL regulated miRNAs by using miRNA high-throughput sequencing of HeLa cells stably expressing double-strand (ds) interfering RNA against NCL or scrambled sequences (sh-NCL or sh-Scr).

2013-02-07 | E-GEOD-44052 | biostudies-arrayexpress

Individual SRC-2 and SRC-3 knock-down in MCF-7 cells

Project description:Experimental aim: identification of SRC-2 and SRC-3-related genes in MCF-7 breast cancer cells. Experimental workflow: 1. shRNA transduction. MCF-7 cells were transduced with a mix of lentiviral particles containing five individual lentiviral pLKO.1-puro short hairpin (sh) RNA plasmids targeting different sequences on SRC-2 or SRC-3 mRNA and a pLKO.1-puro empty vector control. The puromycin selections were maintained for three weeks to obtain cells containing stably integrated shRNA. 2. Sample preparation. RNA was extracted from eight independent replicates expressing the pLKO.1-puro empty shRNA vector (shKTR), from eight replicates of SRC-2 shRNA expressing cells (shSRC-2), and from seven replicates of SRC-3 shRNA expressing cells (shSRC-3). 300 ng of total RNA from each cell sample was biotin-labelled and amplified.

2019-07-01 | E-MTAB-7018 | biostudies-arrayexpress

Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL

Project description:The TLX1 and TLX3 transcription factor oncogenes play an important role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL)1,2. Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This Systems Biology analysis defined TLX1 and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, network structure analysis of this hierarchical network identified RUNX1 as an important mediator of TLX1 and TLX3 induced T-ALL, and predicted a tumor suppressor role for RUNX1 in T-cell transformation. Consistent with these results, we identified recurrent somatic loss of function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 atop of an oncogenic transcriptional network controlling leukemia development, demonstrate power of network analysis to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor suppressor gene in T-ALL. This SuperSeries is composed of the following subset Series: GSE33539: Expression data obtained from ALLSIL cell line GSE33540: Expression data obtained from HPBALL cell line GSE33549: Expression data from mouse T-cell lymphomas

2011-11-08 | E-GEOD-33550 | biostudies-arrayexpress

Phf19 knockdown effect on F9 embryonal carcinoma cells

Project description:PCL family protein Phf19/Pcl3 is one of the accessory components of the PRC2 core complex, and Phf19 is highly expressed in murine ES cells and an ES cell-like embryonic carcinoma cell line, F9 cells. Here we performed microarray analysis of embryonal carcinoma cell line F9 following Phf19 knockdown by shRNA. Knocking down Phf19/Pcl3 in F9 embryonic cells led to derepression of numerous PRC2 direct target genes. 4 sampels including 2 shRNA vector control cell lines and 2 shPhf19 cell lines were used for RNA extraction and Affymetrix mouse 430 2.0 arrays.

2012-12-20 | E-GEOD-42463 | biostudies-arrayexpress

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