Genome wide WT1 binding sites in developing mouse kidneys
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Andreas Schedl
PROVIDER: E-GEOD-58179 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Molecular functions of the Nucleosome Remodeling and Deacetylation (NuRD) complex in the control of gene expression were investigated using an inducible system to direct its assembly in embryonic stem cells. This dataset identifies genome-wide changes in nucleosome positioning at sites of NuRD association.
2018-05-31 | E-MTAB-6807 | biostudies-arrayexpress
Project description:The far-red light (FR) photoreceptor phytochrome A (phyA) contains no DNA binding domain but associates with CHS promoter through its chaperon FHY1 and transcription factors to regulate transcription. Here, we performed a genome-wide identification of phyA targets using a combination of phyA ChIP- and RNA-sequencing methods. Our results indicate that the phyA signaling widely impact gene promoters involved in multiple FR-modulated aspects of plant growth. Furthermore, there was an enrichment of hormones- and stresses-responsive elements in the phyA direct target promoters, indicating that a much broader than expected range of transcription factors are involved in the phyA signaling. To verify our hypothesis that phyA regulates genes other than light-responsive ones through interaction with corresponding transcription factors, we examined the phyA action on one of its direct target gene NAC019, encoding an ABAdependent transcription factor. The phyA signaling cascade, consisting of FHY1 and HY5, not only targets two G-boxes on NAC019 promoter for subsequent transcriptional regulation, but also positively coordinates with ABA response for the root elongation inhibition under FR. Our study provides new insights into how plants rapidly fine-tune their growth strategy upon dynamic light environment by escorting photoreceptors to the promoters of hormones- or stresses-responsive genes for individualized modulation. Four day-old PphyA: phyA-GFP phyA201 transgenic seedlings were irradiated with 3h FR for ChIP with an anti-GFP antibody, which was previously used to detect phyA-GFP upon FR irradiation . Three biologically distinct phyA associated-DNA samples were subjected to library construction and high-throughput Solexa (Illumina) sequencing. An input DNA sample (genomic DNA before antibody immunoprecipitation in ChIP) was sequenced in parallel to exclude false positive signals caused by preferential PCR on certain genomic regions in the process of library construction .
2014-05-06 | E-GEOD-48769 | biostudies-arrayexpress
Project description:We report the genomic sequences bound by the C2H2 transcription factors BLUEJAY and JACKDAW as profiled by chromating immunoprecipitation experiments followed by Illumina high sequencing. Plants were carrying constructs of proteins (translational) fusions of these transcription factors to the yellow fluorescent protein. Gene fusions were expressed under all their genomic regulatory regions using recombineering. The recombineering technique was used to recombine the fluorecent protein at the 3' end of their genomic regions in a JATY clone carrying these genes. Subsequently the JATY clones carrying these translational fusions were introgressed into plants. We performed ChIP on roots grown under standard conditions and fixed with formaldehyde in PBS-EDTA. Sequences bound by BLUEJAY and JACKDAW were immunoprecipitated with a-GFP AbCam290 at 4 °C overnight. Biological replicate samples were make into libraries of ~100 bp insert size and 50 bp of single ends sequenced through Illumina High Sequencing. Two biological replicates of samples of plants expressing the C2H2 transcription factors fused to the yellow fluorescent protein; and of control wild type plants processed through the same protocol.
2015-11-02 | E-GEOD-60011 | biostudies-arrayexpress
Project description:Piwi interacting (pi)RNAs repress diverse transposable elements in the germ cells of metazoans and are essential for fertility in both invertebrates and vertebrates. The precursors of piRNAs are transcribed from distinct genomic regions, the so-called piRNA clusters; however, how piRNA clusters are differentiated from the rest of the genome is not known. To address this question, we studied piRNA biogenesis in two Drosophila virilis strains that show differential ability to generate piRNAs from several genomic regions. We found that active piRNA biogenesis correlates with high levels of histone 3 lysine 9 trimethylation (H3K9me3) over genomic regions that give rise to piRNAs. Furthermore, piRNA biogenesis in the progeny requires the trans-generational inheritance of an epigenetic signal, presumably in form of homologous piRNAs that are generated in the maternal germline and deposited into the oocyte. The inherited piRNAs enhance piRNA biogenesis by installment of H3K9me3 mark on piRNA clusters and by promoting ping-pong processing of homologous transcripts into mature piRNAs. We submitted the resequencing data together with the functional genomic datasets because it was generated with the sole purpose of supporting those. The SRA accession numbers are SRR1536176 and SRR1536175. ChIP-seq against H3K9me3 and Pol2, Total RNA-seq, in Drosophila virilis Strain9 and Strain160 as well as crosses between them
2014-09-01 | E-GEOD-59965 | biostudies-arrayexpress
Project description:The C4-12/Flag.ERβ cell line which stably expressed Flag.ERβ is used to study ERβ genomic functions without ERα interference. Mapping ERβ binding sites in these cells reveals ERβ unique distribution and motif enrichment patterns. Accompanying our mapping results, nascent RNA profiling is performed on cells at the same treatment time. The combined results allow the identification of ERβ target genes. Gene ontology analysis reveals that ERβ targets are enriched in differentiation, development and apoptosis. Concurrently, E2 treatment suppresses proliferation in these cells. Within ERβ binding sites, while the most prevalent binding motif is the canonical ERE, motifs of known ER interactors are also enriched in ERβ binding sites. Moreover, among enriched binding motifs are those of GFI, REST and EBF1, which are unique to ERβ binding sites in these cells. Further characterization confirms the association between EBF1 and the estrogen receptors, which favors the N-terminal region of the receptor. Furthermore, EBF1 negatively regulates ERs at the protein level. In summary, by studying ERβ genomic functions in our cell model, we confirm the anti-proliferative role of ERβ and discover the novel cross talk of ERβ with EBF1 which has various implications in normal physiology. C4-12/Flag.ERβ cells were treated with 10nM E2 for 1 hour then crosslinked with 1% formaldehyde; EtOH treatment was used as control. Crosslinked samples were processed for ChIP-seq and sequenced with Illumina Genome Analyzer II and aligned to hg18. QuEST was used as the peak-calling software, using default parameters recommended to analyze transcription factor ChIP-seq data. The entire ChIP-seq process was performed once on each sample (Vehicle or E2-treated).
2013-06-21 | E-GEOD-48096 | biostudies-arrayexpress
Project description:Genomic DNA was prepared, fragmented, and immunoprecipitated with antibodies specific for 5mC or 5hmC prior to standard sequencing. The neurodegenerative disease known as ataxia-telangiectasia (A-T) is caused by the absence of the ATM (A-T mutated) protein. A long-standing mystery surrounding A-T is why cerebellar Purkinje cells (PCs) appear uniquely vulnerable to ATM-deficiency. Here, we present that 5-hydroxymethylcytosine (5hmC), a newly recognized epigenetic marker found at high levels in neurons, is substantially reduced in human A-T and Atm-/- mouse cerebellar PCs. TET1, an enzyme that converts 5mC to 5hmC, responds to DNA damage. Manipulation of TET1 activity directly affects neuronal cell cycle reentry and cell death after the induction of DNA damage. Quantitative, genome-wide analysis of 5hmC of samples from human cerebellum showed that in ATM-deficiency there is a remarkable genome-wide reduction of 5hmC enrichment at both proximal and distal regulatory elements. These results reveal a role of TET1-mediated 5hmC in DNA damage response, and provide insights into the basis of a PC-specific DNA demethylation alteration in ATM-deficiency. There are two groups, A-T and Control. For each group, cerebellar DNA samples were immunoprecipitated with anti-5mC (n=1) or anti-5hmC (n=3). There were also two replicates of input control for each group.
2015-10-30 | E-GEOD-61133 | biostudies-arrayexpress
Project description:The nature of autoantigens that trigger autoimmune diseases has been much discussed but direct biochemical identification is lacking for most. Addressing this question demands unbiased examination of the self-peptides displayed by a defined autoimmune MHC-II molecule. We have examined the immunopeptidome of the pancreatic islets of the NOD mouse that spontaneously develops autoimmune diabetes based on its MHC-II, the I-Ag7 variant. The relevant peptides that induced early CD4 T cells derived from insulin and C-peptide; these were also found in the MHC-II peptidome of the pancreatic lymph node and spleen. The insulin-derived peptides followed a trajectory from internal processing in beta cells to exocytosis, uptake, and presentation in islets and peripheral sites. Such process not only generated conventional epitopes but also resulted in presentation of post-translationally modified peptides, including deamidated and fused sequences. These analyses reveal the key features of a restricted component in the self-MHC-II peptidome causing autoreactivity.
2020-03-12 | PXD015408 | Pride
Project description:Dynamic changes in histone posttranslational modifications (PTMs) are important regulators of chromatin structure and gene transcription in both normal and disease settings. Herein, we describe a novel signaling mechanism of nitric oxide (â¢NO) by demonstrating its ability to modulate gene expression via alteration of histone PTMs. Having established that â¢NO exposure induced differential expression of approximately 6500 genes, we set out to determine if there was an epigenetic component to their regulation. â¢NO exposure led to alterations in the global levels of acetyl and methyl modifications at numerous lysine residues on core histones H3 and H4. Residues H3K9me2/ac were examined further and determined to have differential distribution at various loci throughout the genome in response to â¢NO. Changes in the enrichment levels of H3K9me2/ac at specific genes correlated with changes in the expression levels of their transcripts. Molecular mechanisms contributing to phenotypic outcomes in â¢NO-associated cancers remain to be well understood since traditional modes of â¢NO-signaling do not explain a large proportion of its impact on tumor cell behavior. Our results reveal that â¢NO drives a significant amount of gene expression changes epigenetically by changing the distribution of numerous histone marks. Cultured cells were treated with 500uM DETA/NO to examine the effects of a physiologically relevant â¢NO concentration on differential distribution of H3K9ac/H3K9me2. A total of two untreated biological replicates and two â¢NO-treated biological replicates were harvested. The untreated samples served as control against which comparisons were made to elucidate â¢NO-mediated changes in the histone landscape.
2015-11-05 | E-GEOD-66318 | biostudies-arrayexpress
Project description:We report the acetylation of lysine residues in the globular domain of H3 (H3K64ac and H3K122ac) marks active gene promoters and also a subset of active enhancers in mouse embryonic stem cells (mESCs), human erythroleukemic cell line (K562). Moreover, we find a novel class of active functional enhancers in ESCs that are marked by H3K122ac but which lack H3K27ac. This work suggests that a more complex analysis of histone acetylation is required to identify enhancers than was previously considered. Examination of histone modifications in mouse ESCs (2 biological replicates) and K562 cells
2016-03-12 | E-GEOD-66023 | biostudies-arrayexpress
Project description:Transcription factor-induced reprogramming of somatic cells to pluripotency is a very inefficient process, probably due to the existence of important epigenetic barriers that are imposed during differentiation and that contribute to preserve cell identity. In an effort to decipher the molecular nature of these barriers, we followed a genome-wide approach, in which we identified macro histone variants (macroH2A) as highly expressed in human somatic cells but downregulated after reprogramming to pluripotency, as well as strongly induced during differentiation. Knock down of macro histone variants in human keratinocytes increased the efficiency of reprogramming to pluripotency, while overexpression had opposite effects. Genome-wide occupancy profiles show that in human keratinocytes macroH2A.1 preferentially occupies genes that are expressed at low levels and are marked with H3K27me3, including pluripotency-related genes and bivalent developmental regulators, at which its presence prevents the regain of H3K4me2 during reprogramming, over imposing an additional layer of repression that preserves cell identity. Gemone wide occupancy of HA:macroH2A.1 in human keratinocytes
2013-04-03 | E-GEOD-44400 | biostudies-arrayexpress