Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RING1B calibrated ChIP-seq (cChIPseq) datasets for control mESCs and an Scc1-AID auxin-inducible degron.

ABSTRACT: We examined 3D chromatin structure in the absence of cohesin (Scc1-AID auxin-inducible degron) and a control line (E14-Tir1) and found that PRC1 core promoter component RING1B was one of the most enriched proteins. Hence, we performed calibrated ChIP-seq experiments on the control (E14-Tir1) and the Scc1-AID mESC lines with a spike in of HEK293 human cells to further study this relationship.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Angelika Feldmann

PROVIDER: E-MTAB-7817 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells

Project description:The aim of the experiment was to gain a higher resolution for specific regions of interest to complement the Hi-C results. Capture-C experiments were performed on four-inducible degrons for Scc1, Ringb, Ring1b-Scc1 and CTCF, and Tir1 control, always in triplicates (three biological replicates per condition).

2020-01-23 | E-MTAB-7840 | biostudies-arrayexpress

Calibrated total RNAseq (cRNA-seq) of E14_Scc1_AID mESCs mixed with Drosophila SG4 cells with and without a 6-hour auxin treatment

Project description:We performed calibrated total RNAseq on mESC (Scc1-AID) for both untreated and treated cells with a 6-hour auxin exposure to assess the effects of cohesin removal on gene expression. For calibration purposes 2x10ˆ6 Drosophila SG4 cells were spiked in.

2020-01-23 | E-MTAB-7818 | biostudies-arrayexpress

DNA double-strand breaks and 3D chromatin conformation (Hi-C, 4C-seq, ChIP-seq)

Project description:DNA Double-Strand Breaks (DSBs) are highly detrimental since they can lead to mutations and chromosomes rearrangements (amplification, deletion, translocation and chromosome loss). Here, we set to assess the tridimensional genome organization around DSBs and its role in DSB repair foci formation. We performed Hi-C experiments before and after DSB induction and upon ctrl or SCC1 depletion, 4C-seq experiments before and after DSB induction and upon cohesin (SCC1) depletion or ATM inhibition. We also performed ChIP-seq of pATM(S1981), CTCF, P-SMC3(S1083), MDC1 and a calibrated ChIP-seq of SCC1 with or without damage. ChIP-chip of SMC3 (S1083) and SMC1 (S966) were used to show the recruitment of these marks on DNA repair foci. ChIP-chip of gammaH2AX was realized upon SCC1 depletion and ChIP-seq of gammaH2AX was realized upon SCC1 or WAPL to show the role of the cohesin complex in gammaH2AX foci formation. ChIP-seq of gammaH2AX was realized upon ATM or ATR inhibition to show that ATM is the major kinase that phosphorylates H2AX at clean breaks in human cells.

2021-01-29 | E-MTAB-8851 | biostudies-arrayexpress

Analyses of blue light (BL) and CRY-regualted genes and genes dependent on auxin receptors by RNA-seq

Project description:Total RNA was extracted from samples including dark-grown WT and tir1 afb123, blue light-grown WT and cry1 cry2 seedlings in continuous conditions for 4.5 days and subjected to high throughput sequencing. Light and auxin co-regulate a variety of developmental processes. This study reveals the molecular basis for light and auxin crosstalk by analyzing gene expression profile under control of both signals. mRNA from dark-grown WT, BL-grown WT, BL-grown BL photoreceptors, and dark-grown auxin receptors was sequenced to analyze the genes regulated by CRY-mediated BL signaling and TIR1/AFBs-mediated auxin signaling.

2016-06-15 | E-GEOD-58552 | biostudies-arrayexpress

Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [ChIP-seq_Input]

Project description:Polycomb group (PcG) proteins are required for normal differentiation and development, and their activity is found deregulated in cancer. PcG proteins are involved in gene silencing, however, whether they initiate or maintain transcriptional repression is a subject of debate. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs), and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of un-transcribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to non-transcribed CGI genes to maintain their silenced state and to protect cell identity. Input from ChIP-seq experiment in Mus musculus wild-type E14 Embryonic Stem Cells.

2014-07-03 | E-GEOD-58022 | biostudies-arrayexpress

Six in situ Hi-C libraries of control and mESC auxin-inducible degrons for Scc1 and Ring1b.

Project description:In this experiment, we've examined chromatin conformation differences of E14 mESC against cohesin and Ring1b degrons. We performed a modified in situ Hi-C protocol from (Rao et al., 2014) that can be found in detail at (Díaz et al., 2018). Samples were digested with MboI restriction enzyme. The aim of the experiment was to characterize the role of cohesin and polycomb on the 3D structure of mouse chromatin.

2020-01-23 | E-MTAB-7816 | biostudies-arrayexpress

ATAC-seq of wild-type, Pbx1/Pbx2 double-knockout and pMsgn1-mut EpiSCs differentiated in vitro to pre-somitic mesoderm in the first 48 hours of differentiation.

Project description:In vertebrates, body axis elongation is fuelled by bipotent neuromesodermal progenitors (NMPs), which support the development of both spinal cord and paraxial mesoderm (PM). WNT signalling sustains both NMP expansion and PM differentiation, but the mechanism by which it distinguishes between these alternative fates is unknown. HOX transcription factors have been historically implicated in axial elongation, with their sequential activation playing a fundamental role in timing PM development. PBX1 and PBX2 are obligate anterior HOX cofactors, and therefore they represent prominent candidates for controlling the distinct response to individual HOX factors. In our work, we have demonstrated that PBX/HOX complexes establish a permissive chromatin landscape for de novo recruitment of the WNT-effector LEF1 on PM genes, including the master regulator Mesogenin1 (Msgn1). To assess the PBX-dependent changes in chromatin accessibility during PM differentiation, we performed ATAC-seq of wild-type (WT) and Pbx1/Pbx2 double-knockout (Pbx1/2-DKO) EpiSCs differentiated in vitro to pre-somitic mesoderm (PSM) at different time-points (EpiSCs, 6 hours, 12 hours, 24 hours, 36 hours, 48 hours). To assess the direct consequence of PBX/HOX binding on chromatin accessibility, we employed the CRISPR/Cas9 technology to generate lines carrying base-pair substitutions on the Msgn1 promoter (pMsgn1-mut) that abrogate the recruitment of PBX/HOX complexes, and we performed ATAC-seq of pMsgn1-mut EpiSCs differentiated in vitro to PSM at different time-points (12 hours, 24 hours, 36 hours, 48 hours).

2021-07-21 | E-MTAB-9776 | biostudies-arrayexpress

Calibrating ChIP-seq with nucleosomal internal standards to measure histone modification density genome-wide

Project description:Despite serving as a central experimental technique in epigenetics research, chromatin immunoprecipitation (ChIP) suffers from several serious drawbacks: it is a relative measurement untethered to any external scale that obviates fair comparison amongst experiments; it employs antibody reagents that have differing affinity and specificity for target epitopes, which are in turn variable in abundance; and it is frequently not reproducible. To address these problems, we developed internal standard calibrated ChIP (ICeChIP), a method of spiking a native chromatin sample with nucleosomes reconstituted from recombinant and semisynthetic histones on barcoded DNA prior to immunoprecipitation. ICeChIP measures local histone modification densities on a biologically meaningful scale, enabling unbiased trans-experimental comparisons and revealing a correlation between the apparent symmetry of H3K4me3 in promoter nucleosomes and gene expression. Direct in situ assessment of immunoprecipitation accommodates for a number of experimental pitfalls, and provides a critical examination of untested assumptions inherent in conventional ChIP. Examination of spiked-in semi-synthetic nucleosomes in ICeChIP-seq experiments performed for HEK293, mESC E14 and DM S2 cell line

2015-05-07 | E-GEOD-60378 | biostudies-arrayexpress

Bulk ATAC-Sequencing of isolated spermatocytes from testis tissue from B6/CAST F1 hybrid mice

Project description:We performed profiling of allele-specific chromatin accessibility profiling in mouse spermatocytes. To this end, we isolated tetraploid spermatocytes using FACS-sorting from F1 crosses of the C57B6J and CAST/EiJ strains. We then performed ATAC-Seq (Corces et al. 2017) and analyzed allele-specific chromatin accessibility.

2023-12-01 | E-MTAB-12685 | biostudies-arrayexpress

Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [RNA-seq_differentiation]

Project description:Polycomb group (PcG) proteins are required for normal differentiation and development, and their activity is found deregulated in cancer. PcG proteins are involved in gene silencing, however, whether they initiate or maintain transcriptional repression is a subject of debate. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs), and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of un-transcribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to non-transcribed CGI genes to maintain their silenced state and to protect cell identity. RNA-seq time-course experiments during in vitro differentiation (0h, 24h, 48h and 72h) of Mus musculus wild-type E14 and Suz12 knock-out Embryonic Stem Cells with two biological replicates per condition.

2014-07-03 | E-GEOD-58017 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data