FOG-1-independent transcripition by GATA-1(V205G) in G1E cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE6958 | GEO | 2007/03/05
SECONDARY ACCESSION(S): PRJNA99321
REPOSITORIES: GEO
Similar Datasets
Project description:Identification of genes regulated by GATA-1 independent of the cofactor FOG-1. Experiment Overall Design: A conditionally activated FOG-1-binding defective mutant of GATA-1, ER-GATA-1(V205G), was expressed in GATA-1-null G1E cells. Transcipt levels were compared in cells untreated or treated with estradiol to activate the GATA-1 mutant.
2008-06-15 | E-GEOD-6958 | biostudies-arrayexpress
Project description:We explored the role of FOG-1 in GATA-1 transcriptional regulation of megakaryocyte differentiation through expression of wild-type GATA-1 and the FOG-binding mutant of GATA-1 (GATA-1^V205G) in G1ME cells.
2012-03-05 | GSE35695 | GEO
Project description:The transcription factor GATA-1 is essential for erythroid and megakaryocytic cell differentiation and maturation. Previous reports show that GATA-1 is modulated through acetylation modification and through FOG-1 mediated indirect intereaction with HDAC1/2 containing NuRD corepressor complexes. In this study, we found that NuRD does not deacetylate GATA-1. However, HDAC1 alone can efficiently deacetylates GATA-1 and the direct interaction of HDAC1 and GATA-1 is required for the deacetylation. Two arginines within GATA-1 linker region are important for this interaction and arginine to alanine mutations (2RA mutant) largely reduces GATA-1 binding to HDAC1 in FOG-1 independent manner. GATA-1 2RA mutant were then introduced into G1E cells, a GATA-1-null erythroid progenitor cells. The 2RA mutant is acetylated but fails to induce erythroid differentiation. Gene expression analysis shows that GATA-1 2RA mutant affects GATA-1 function in both GATA-1 activated and repressed genes. The gene expression pattern partially overlap with gene expression profile of GATA-1V205M, a GATA-1 mutant with defective FOG-1 binding. ChIP-seq analysis further reveal that 2RA mutation largely reduced GATA-1 chromatin binding, most profoundly at gene promoter regions. HDAC1 recruitment on those promoters are also strongly reduced. These results revealed that GATA-1 recruits HDAC1 to GATA-1 regulated gene promoters and HDAC1 is required for GATA-1 mediated transcription regulation.
2021-09-29 | GSE161608 | GEO
Project description:We report ChIP-Seq data for GATA-1 and the FOG-binding mutant of GATA-1 (GATA-1^V205G) in G1ME cells, a Gata1-null cell line with both erythroid and megakaryocytic differentiation potential. We introduced HA-tagged GATA-1 or V205G into G1ME cells via retroviral transduction. The cells were crosslinked at 48h post-transduction, and an HA antibody was used for chromatin immunoprecipitation (ChIP). ChIP and input samples were sequenced on Illumina GAII high-throughput sequencer. The data reveal GATA-1-specific and V205G-specific bidning sites, indicating that FOG-1 both faacilitates and prohibits GATA-1 chromatin occupancy in a context-dependent manner.
2012-07-30 | GSE35644 | GEO
Project description:We report ChIP-Seq data for GATA-1 and the FOG-binding mutant of GATA-1 (GATA-1^V205G) in G1ME cells, a Gata1-null cell line with both erythroid and megakaryocytic differentiation potential. We introduced HA-tagged GATA-1 or V205G into G1ME cells via retroviral transduction. The cells were crosslinked at 48h post-transduction, and an HA antibody was used for chromatin immunoprecipitation (ChIP). ChIP and input samples were sequenced on Illumina GAII high-throughput sequencer. The data reveal GATA-1-specific and V205G-specific bidning sites, indicating that FOG-1 both faacilitates and prohibits GATA-1 chromatin occupancy in a context-dependent manner. Examinaton of chromatin occupancy of GATA-1 anda FOG-binding mutant of GATA-1 in G1ME cells cultured in TPO.
2012-07-30 | E-GEOD-35644 | biostudies-arrayexpress
Project description:Heme-regulated eIF2α kinase (HRI) is essential for the survival of erythroid precursors in iron and heme deficiency and it also plays a protective role in red blood cell diseases of erythroid protoporphyria and β-thalassemia. In this study, we demonstrated for the first time the impairment of GATA-1 and Fog-1 expressions in iron deficiency and the impairment of GATA-1 expression in β-thalassemia. Furthermore, HRI is necessary to maintain the GATA-1/Fog-1 induced functions in erythroid differentiation, cell cycle and cell survival by sustaining both expressions of GATA-1 and Fog-1 in iron deficiency and in β-thalassemia. Keywords: Genetic modification
2009-06-30 | GSE6808 | GEO
Project description:The establishment and maintenance of cell type-specific transcriptional programs require an ensemble of broadly expressed chromatin remodeling and modifying enzymes. Many questions remain unanswered regarding the contributions of these enzymes to specialized genetic networks that control critical processes such as lineage commitment and cellular differentiation. We have been addressing this problem in the context of erythrocyte development driven by the transcription factor GATA-1 and its coregulator Friend of GATA-1 (FOG-1). As certain GATA-1 target genes have little to no FOG-1 requirement for expression, presumably additional coregulators can mediate GATA-1 function. Using a genetic complementation assay and RNA interference in GATA-1-null cells, we demonstrate a vital link between GATA-1 and the histone H4 lysine 20 methyltransferase PR-Set7/SetD8 (SetD8). GATA-1 selectively induced H4 monomethylated lysine 20 at repressed, but not activated, loci, and endogenous SetD8 mediated GATA-1-dependent repression of a cohort of its target genes. GATA-1 utilized different combinations of SetD8, FOG-1, and the FOG-1-interacting Nucleosome Remodeling and Deacetylase (NuRD) complex component Mi2b to repress distinct target genes. Implicating SetD8 as a context-dependent GATA-1 corepressor expands the repertoire of coregulators mediating establishment/maintenance of the erythroid cell genetic network and provides a biological framework for dissecting the cell type-specific functions of this important coregulator. We propose a coregulator matrix model in which distinct combinations of chromatin regulators are required at different GATA-1 target genes, and the unique attributes of the target loci mandate these combinations.
2013-07-24 | GSE49174 | GEO
Project description:We explored the role of FOG-1 in GATA-1 transcriptional regulation of megakaryocyte differentiation through expression of wild-type GATA-1 and the FOG-binding mutant of GATA-1 (GATA-1^V205G) in G1ME cells. G1ME cells were derived from Gata1-null mouse ES cells and have both megakaryocyte and erythrocyte differentiation potential upon reconstitution of GATA-1 expression (Stachura 2006). HA-tagged wild-type or mutant GATA-1 were expressed in G1ME cells grown in TPO via retroviral transductions. The cells were sorted for GFP positivity 68 hours post-transduction and then were allowed to recover in normal growth medium for 4h. Total RNA was then isolated using RNeasy kit from Qiagen 72 hours post-transduction.
2012-03-05 | E-GEOD-35695 | biostudies-arrayexpress
Project description:The establishment and maintenance of cell type-specific transcriptional programs require an ensemble of broadly expressed chromatin remodeling and modifying enzymes. Many questions remain unanswered regarding the contributions of these enzymes to specialized genetic networks that control critical processes such as lineage commitment and cellular differentiation. We have been addressing this problem in the context of erythrocyte development driven by the transcription factor GATA-1 and its coregulator Friend of GATA-1 (FOG-1). As certain GATA-1 target genes have little to no FOG-1 requirement for expression, presumably additional coregulators can mediate GATA-1 function. Using a genetic complementation assay and RNA interference in GATA-1-null cells, we demonstrate a vital link between GATA-1 and the histone H4 lysine 20 methyltransferase PR-Set7/SetD8 (SetD8). GATA-1 selectively induced H4 monomethylated lysine 20 at repressed, but not activated, loci, and endogenous SetD8 mediated GATA-1-dependent repression of a cohort of its target genes. GATA-1 utilized different combinations of SetD8, FOG-1, and the FOG-1-interacting Nucleosome Remodeling and Deacetylase (NuRD) complex component Mi2b to repress distinct target genes. Implicating SetD8 as a context-dependent GATA-1 corepressor expands the repertoire of coregulators mediating establishment/maintenance of the erythroid cell genetic network and provides a biological framework for dissecting the cell type-specific functions of this important coregulator. We propose a coregulator matrix model in which distinct combinations of chromatin regulators are required at different GATA-1 target genes, and the unique attributes of the target loci mandate these combinations. 3 SetD8 knockdown samples were compared to 3 control samples
2013-07-24 | E-GEOD-49174 | biostudies-arrayexpress
Project description:FOG-1/CPEB and FOG-3/Tob are the terminal regulators of the sex determination in C. elegans germ cells. CPEB and Tob proteins are both translational regulators. To investigate how FOG-1 and FOG-3 regulate germ cell sex determination we sought to identify the target mRNAs. We used transgenic epitope tagged animals (3xMyc::FOG-1 and FOG-3::3xFLAG). To identify the mRNA targets of FOG-1/CPEB and FOG-3/Tob on a genome wide scale we used RNA immunoprecipitation followed by microarray analysis. We found 81 putative mRNA targets of FOG-1 and 722 putative targets of FOG-3. 76 target mRNAs were common to both FOG-1 and FOG-3.
2015-12-14 | GSE73070 | GEO