Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-77576
PROVIDER: PRJNA310767 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Complex Interdependence Regulates Heterotypic Transcription Factor Distribution and Coordinates Cardiogenesis [microarray]
| PRJNA310968 | ENA
Project description:Complex Interdependence Regulates Heterotypic Transcription Factor Distribution and Coordinates Cardiogenesis [RNA-Seq]
| PRJNA310768 | ENA
Project description:Dominant mutations in cardiac transcription factor genes cause human inherited congenital heart defects (CHDs), but their molecular basis is not understood. Transcription factors and Brg1/Brm-associated factor (BAF) chromatin remodeling complex interactions suggest potential mechanisms, but the role of BAF complexes in cardiogenesis is not known. Here we show that dosage of Brg1 is critical for mouse and zebrafish cardiogenesis. Disrupting the balance between Brg1 and disease-causing cardiac transcription factors, including Tbx5, Tbx20, and Nkx2-5, causes severe cardiac anomalies, revealing an essential allelic balance between Brg1 and these cardiac transcription factor genes. This suggests that relative levels of transcription factors and BAF complexes are important for heart development, which is supported by reduced occupancy of Brg1 at cardiac genes in Tbx5 haploinsufficient hearts. Our results reveal complex dosage-sensitive interdependence between transcription factors and BAF complexes, providing a potential mechanism underlying transcription factor haploinsufficiency, with implications for multigenic inheritance of CHDs. We performed transcriptional profiling of E11.5 hearts from mice heterozygous for deletions of Brg1, Tbx5, or Nkx2-5, and mice that were compound heterozygotes for Brg1 and each transcription factor gene (Tbx5 and Nkx2-5).
2010-12-22 | E-GEOD-26191 | biostudies-arrayexpress
Project description:Dominant mutations in cardiac transcription factor genes cause human inherited congenital heart defects (CHDs), but their molecular basis is not understood. Transcription factors and Brg1/Brm-associated factor (BAF) chromatin remodeling complex interactions suggest potential mechanisms, but the role of BAF complexes in cardiogenesis is not known. Here we show that dosage of Brg1 is critical for mouse and zebrafish cardiogenesis. Disrupting the balance between Brg1 and disease-causing cardiac transcription factors, including Tbx5, Tbx20, and Nkx2-5, causes severe cardiac anomalies, revealing an essential allelic balance between Brg1 and these cardiac transcription factor genes. This suggests that relative levels of transcription factors and BAF complexes are important for heart development, which is supported by reduced occupancy of Brg1 at cardiac genes in Tbx5 haploinsufficient hearts. Our results reveal complex dosage-sensitive interdependence between transcription factors and BAF complexes, providing a potential mechanism underlying transcription factor haploinsufficiency, with implications for multigenic inheritance of CHDs.
2010-12-22 | GSE26191 | GEO
Project description:The goal of the ChIP-seq study was to investigate the distribution of the TATA-binding protein (TBP) across the human genome. TBP is the DNA-binding subunit of the basal transcription factor TFIID for RNA polymerase II (pol II) and it also participates in other complexes for the other RNA polymerase. The BTAF1 ATPase forms a stable complex with TBP and regulates its activity in pol II transcription. BTAF1 is believed to mobilize TBP from promoter and non-promoter sites. To test this hypothesis, TBP ChIP samples were prepared from human HeLa cervix carcinoma cells after knock-down of BTAF1 expression and compared to HeLa cells with a control knock-down of GAPDH. GAPDH is a cytosolic enzyme that participates in glycolysis, and its inactivation is not expected to affect the genomic distribution of TBP, and acts as negative control. ChIP samples were sequenced using SOLiD technology along with the INPUT sample to normalize the distribution of background signals within each of the two chromatin samples. 2 ChIP samples + one input sample
2010-03-02 | E-GEOD-17937 | biostudies-arrayexpress
Project description:Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis [ChIP-Seq]
| PRJNA339028 | ENA
Project description:Rationale: Cardiogenesis is regulated by a complex interplay between transcription factors and chromatin-modifying enzymes. However, little is known about how these interactions regulate the transition from mesodermal precursors to cardiac progenitor cells (CPCs). Objective: To identify novel regulators of mesodermal cardiac lineage commitment. Methods and Results: We performed a bioinformatic-based transcription factor-binding site analysis on upstream promoter regions of genes that are enriched in ES cell-derived CPCs. From 32 candidate transcription factors screened, we found that YY1, a repressor of sarcomeric gene expression, is present in CPCs in vivo. Interestingly, we uncovered the ability of YY1 to transcriptionally activate Nkx2.5, a key marker of early cardiogenic commitment. YY1 regulates Nkx2.5 expression via a 2.1 kb cardiac-specific enhancer as demonstrated by in vitro luciferase-based assays and in vivo chromatin immunoprecipitation (ChIP) and genome-wide sequencing analysis. Furthermore, the ability of YY1 to activate Nkx2.5 expression depends on its cooperative interaction with GATA4 at a nearby chromatin. Cardiac mesoderm-specific loss-of-function of YY1 resulted in early embryonic lethality. This was corroborated in vitro by ES cell-based assays where we show that the over-expression of YY1 enhanced the cardiogenic differentiation ES cells into CPCs in a cell autonomous manner. Conclusion: These results demonstrate an essential and unexpected role for YY1 to promote cardiogenesis as a transcriptional activator of Nkx2.5 and other CPC-enriched genes. We report the identification of putative YY1 target genes in cardiac progenitor cells (CPCs). Two samples of independently FACS-purified eGFP+ CPCs were examined against the input.
2013-06-01 | E-GEOD-35370 | biostudies-arrayexpress
Project description:The goal of the ChIP-seq study was to investigate the distribution of the TATA-binding protein (TBP) across the human genome. TBP is the DNA-binding subunit of the basal transcription factor TFIID for RNA polymerase II (pol II) and it also participates in other complexes for the other RNA polymerase. The BTAF1 ATPase forms a stable complex with TBP and regulates its activity in pol II transcription. BTAF1 is believed to mobilize TBP from promoter and non-promoter sites. To test this hypothesis, TBP ChIP samples were prepared from human HeLa cervix carcinoma cells after knock-down of BTAF1 expression and compared to HeLa cells with a control knock-down of GAPDH. GAPDH is a cytosolic enzyme that participates in glycolysis, and its inactivation is not expected to affect the genomic distribution of TBP, and acts as negative control. ChIP samples were sequenced using SOLiD technology along with the INPUT sample to normalize the distribution of background signals within each of the two chromatin samples.
2010-03-02 | GSE17937 | GEO
Project description:While it has been clearly established that well positioned H2A.Z-containing nucleosomes flank the nucleosome depleted region (NDR) at the transcriptional start site (TSS) of active mammalian genes, how this chromatin-based information is transmitted through the cell cycle is unknown. We show here that in trophoblast stem (TS) cells, the level of H2A.Z at promoters decreases during S phase coinciding with homotypic (H2A.Z/H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z/H2A). Surprisingly, these nucleosomes remain heterotypic at M phase. At the TSS, we identify an unstable heterotypic H2A.Z-containing nucleosome in G1 which, strikingly, is lost following DNA replication. These dynamic changes in H2A.Z at the TSS mirror a global expansion of the NDR at S and M which, unexpectedly, is unrelated to transcriptional activity. Coincident with the loss of H2A.Z at promoters, it is targeted to the centromere when mitosis begins We performed ChIP-Seq experiments (on mouse Trophoblast Stem cells arrested at G1; S and M stages of thecell cycle) using antibodies against histone variant H2A.Z and sequentional ChIP-re-ChIP-Seq experiments using H2A.Z antibody and H2A antibody in sequence. Combining those data sets with microarray gene expression expression data allowed us to see H2A.Z distribution over promoters of mouse coding genes in cell cycle dependant manner. Interestingly, Input also showed cell-cycle dependent effects, but histone H3 could be used as a cell-cycle independent normalisation factor. We also performed ChIP-seq with a CTCF pull-down to investigate its cell-cycle dependent relationship with heterochromatin.
2012-11-23 | E-GEOD-41371 | biostudies-arrayexpress