A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Ross Hardison
PROVIDER: E-GEOD-83293 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous). Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.
2016-06-15 | E-GEOD-83255 | biostudies-arrayexpress
Project description:ChIP-seq of total Pol II in G1E ER4 cell line at time points after mitosis. Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.
2016-06-15 | E-GEOD-83263 | biostudies-arrayexpress
Project description:Erythroid development and differentiation from multiprogenitor cells to red blood cells requires precise transcriptional regulation. Key erythroid transcription factors, GATA1 and TAL1, co-operate, along with other proteins, to regulate many aspects of this process. How GATA1 and TAL1 are positionally organized with respect to each other and their cognate DNA binding site across the mouse genome remains unclear. We applied high resolution ChIP-exo to GATA1 and TAL1 to study their positional organization across the mouse genome during GATA1-dependent maturation. Two complementary methods, MultiGPS and peak-pairing, were used to determine high confidence binding locations by ChIP-exo. We identified ~10,000 GATA1 and ~15,000 TAL1 locations, which were essentially confirmed by ChIP-seq. Of these, ~4,000 locations were bound by both GATA1 and TAL1. About three-quarters of these were tightly linked (<40 bp away) to a partial E-box located 7-8 bp upstream of a WGATAA motif. Both TAL1 and GATA1 generated distinct characteristic ChIP-exo peaks around WGATAA motifs, that reflect on their positional arrangement within a complex. We show that TAL1 and GATA1 form a precisely organized complex at a compound motif consisting of a TG 7-8 bp upstream of a WGATAA motif across thousands of genomic locations. Genome wide analysis of GATA1 and TAL1 in G1E and G1E-ER4 cells using ChIP-exo experiments
2015-09-17 | E-GEOD-68964 | biostudies-arrayexpress
Project description:Missense mutations in transcription factor GATA1 underlie several distinct forms of anemia and thrombocytopenia. Clinical severity depends on the site and type of substitution, and distinct substiutions of the same residue produce disparate phenotypes. To investigate the effect of GATA1 missense mutations on erythroid differentiation we expressed conditionally activated wild type or mutant versions of GATA1 in GATA1-null G1E cells. We used gene expression microarrays to explore how GATA1 missense mutations affect erythroid transcription programs. GATA1-null G1E cells ectopically expressing conditionally activated versions of GATA1 (GATA1-ER, GATA1(R216Q)-ER, GATA1(R216W)-ER, GATA1(D218G)-ER, or GATA1(D218Y)-ER) were treated with estradiol for 24 hours to initiate erythroid differentiation. Total RNA from treated cells was extracted for Affymetrix microarray. All data were generated from three biological replicates. Transcript levels were compared in wild type vs. mutant lines.
2013-03-04 | E-GEOD-43356 | biostudies-arrayexpress
Project description:Tissue-specific transcription patterns are preserved throughout cell divisions to maintain lineage fidelity. We investigated whether transcription factor GATA1 plays a role in transmitting hematopoietic gene expression programs through mitosis when transcription is transiently silenced. Live cell imaging revealed that a fraction of GATA1 is retained focally within mitotic chromatin. ChIP-seq of highly purified mitotic cells uncovered that key hematopoietic regulatory genes are occupied by GATA1 in mitosis. The GATA1 co- regulators FOG1 and TAL1 dissociate from mitotic chromatin, suggesting that GATA1 functions as platform for their postmitotic recruitment. Mitotic GATA1 target genes tend to re-activate more rapidly upon entry into G1 than genes from which GATA1 dissociates. A novel system designed to destroy GATA1 specifically during mitosis revealed that mitotic occupancy is required for rapid target gene reactivation. These studies suggest a requirement of mitotic “bookmarking” by GATA1 for the faithful propagation of cell type-specific transcription programs through cell division GATA1 occupancy profiles in mitotic G1E-ER4 +E2 cells generated by ChIP-sequencing. ChIP input DNA was sequenced as control. Previously reported (GSE18164) GATA1 occupancy in asynchrnous G1E-ER4 +E2 cells was analysed and compared with mitotic GATA1 occupancy.
2012-08-17 | E-GEOD-36589 | biostudies-arrayexpress
Project description:we mapped the locations of DNA segments occupied by GATA1 using chromatin immunoprecipitation (ChIP). We have produced genome-wide GATA1 ChIP datasets after restoration and activation in G1E-ER4 cells. we employed the sequence census methodology of ChIP-seq , using Illumina GA2 technology to produce 23 million reads (36 nucleotides long) uniquely mapped to the mouse genome (mm8 assembly) for the GATA1 ChIP DNA and 15 million mapped reads for the input DNA Examination of transcription factor GATA1 occupancy
2009-09-19 | E-GEOD-18164 | biostudies-arrayexpress
Project description:Mitosis entails global alterations to chromosome structure and nuclear architecture, concomitant with transient silencing of transcription. How cells transmit transcriptional states through mitosis remains incompletely understood. While many nuclear factors dissociate from mitotic chromosomes, the observation that certain nuclear factors and chromatin features remain associated with individual loci during mitosis originated the hypothesis that they could provide transcriptional memory through mitosis. To obtain the first genome-wide view of the dynamics of chromatin structure during mitosis, we compared the DNase sensitivity of interphase and mitotic chromatin at two stages of cellular maturation in a rapidly dividingmurine erythroblastmodel. Despite global chromosome condensation visible during mitosis at the microscopic level, the chromatin accessibility landscape is largely unaltered. However, mitotic chromatin accessibility is locally dynamic, with individual loci maintaining none, some, or all of their interphase accessibility. Mitotic reduction in accessibility occurs primarily within narrow, highly hypersensitive sites that frequently coincide with transcription factor binding sites, whereas broader domains of moderate accessibility tend to be more stable. In mitosis, proximal promoters generally maintain their accessibility, whereas distal regulatory elements preferentially lose accessibility. Promoters with the highest degree of accessibility preservation in mitosis tend to also be accessible across many murine tissues in interphase. Transcription factor GATA1 exerts site-specific changes in interphase accessibility that are most pronounced at distal regulatory elements, but does not visibly influence mitotic accessibility. We conclude that features of open chromatin are remarkably stable through mitosis and are modulated at the level of individual genes and regulatory elements. Dnase-Seq data is integrated with Chip-seq [GSE36589, GSE30142] and RNA-seq to examine epigentic changes in mitosis. We performed DNase-seq on two cell lines, G1E and G1E-ER4, both on an asynchronus population, and on a sample of cells in mitosis; each of the 4 experiments in triplicate.
2014-10-01 | E-GEOD-61885 | biostudies-arrayexpress
Project description:Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration Mouse G1E or G1ER cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total Smad1 (Santa Cruz SC-7965), Gata1 (Santa Cruz SC-265), or Gata2 (Santa Cruz SC-9008). This represents the Mouse ChIP-seq portion of this dataset.
2011-10-07 | E-GEOD-29193 | biostudies-arrayexpress
Project description:Analysis of erythroid differentiation using Gata1 gene-disrupted G1E ER4 clone cells. Estradiol addition activates an ectopically expressed Gata-1-estrogen receptor fusion protein, triggering synchronous differentiation. 30 hour time course corresponds roughly to late burst-forming unit-erythroid stage (t=0 hrs) through orthochromatic erythroblast stage (t=30 hrs). Experiment Overall Design: G1E ER4 cells cultured in G1E medium were treated at 6 time points with estradiol to initiate erythroid differentiation by activating Gata1 transcription factor and total RNAs from treated cells were extracted for microarray experiment. The erythroid differentiation status was confirmed by cell pellet color and expression of microRNA miR451. The design was similar to an earlier studies (Welch, J. J., Watts, J. A., Vakoc, C. R., Yao, Y., Wang, H., Hardison, R. C., Blobel, G. A., Chodosh, L. A., and Weiss, M. J. (2004)). Global regulation of erythroid gene expression by transcription factor GATA-1. Blood 104, 3136-3147), except that a more recent version of Affymetric chip was used to acheive greater transcriptome coverage.
2009-09-18 | E-GEOD-18042 | biostudies-arrayexpress
Project description:We used chromatin immunoprecipitation sequencing (ChIP-seq) to compare genome-wide binding profiles of GATA1fl and GATA1s in G1ME cells, which are immortalized, developmentally arrested megakaryocyte-erythroid progenitors (MEPs) derived from in vitro differentiation of murine Gata1- ES cells. Although the truncation in GATA1s leaves the DNA binding domain intact, GATA1s fails to broadly occupy erythroid specific regulatory regions. These observations point to lineage specific co-factor associations essential for normal chromatin occupancy and provide mechanistic insights into how GATA1s mutations cause human disease. We performed ChIP-seq on G1ME cells 42 hours after retroviral transfer of HA-tagged full-length GATA1 (GATA1fl) or GATA1s cDNAs (2 replicates each). At this time point, there was no apparent difference in the cell surface phenotypes between GATA1fl and GATA1s-expressing cells. For each ChIP-seq replicate we obtained a matching input sample (non-ChIP DNA) as a control.
2015-01-26 | E-GEOD-61932 | biostudies-arrayexpress