Lineage selective cardiac GATA4 chromatin occupancy [embryo]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA656292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12424703.fastq.gz | Fastqsanger.gz | |||
| SRR12424704.fastq.gz | Fastqsanger.gz | |||
| SRR12424705.fastq.gz | Fastqsanger.gz | |||
| SRR12424706.fastq.gz | Fastqsanger.gz | |||
| SRR12424707.fastq.gz | Fastqsanger.gz |
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Project description:We used cre-directed biotinylation of a GATA4 knockin allele with an AviTag epitope tag to measure GATA4 chromatin occupancy in endocardial and cardiomyocyte lineages in the E12.5 heart. These data are complemented by lineage selective measurement of gene expression and chromatin accessibility. Cardiomyocyte accessibility and gene expression data were reported in GSE124008.
2021-07-01 | GSE156001 | GEO
Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.
2014-01-01 | E-GEOD-52317 | biostudies-arrayexpress
Project description:Here, we show that adult cardiac fibroblasts express the cardiomyocyte transcription factors GATA-4 and GATA-6 to promote adaptive remodeling in pressure overload induced cardiac hypertrophy. Using a mouse model with specific single or double deletion of Gata4 and Gata6 in stress activated fibroblasts, we found a reduced myocardial capillarization in mice with Gata4/6 double deletion following pressure overload, while single deletion of Gata4 or Gata6 had no effect. Importantly, we confirmed the reduced angiogenic response using an in vitro co-culture system with Gata4/6 deleted cardiac fibroblast and endothelial cells. A comprehensive RNA-sequencing analysis revealed an upregulation of anti-angiogenic genes upon Gata4/6 deletion in fibroblasts, and siRNA mediated downregulation of these genes restored endothelial cell growth. In conclusion, we identified a novel role for the cardiac transcription factors GATA4 and GATA6 in heart fibroblasts, where both proteins act in concert to promote myocardial capillarization and heart function by directing intercellular crosstalk.
2021-04-28 | GSE155358 | GEO
Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes.
2014-01-01 | GSE52317 | GEO
Project description:Through integration of GATA4 genome-wide occupancy and RNA-seq dataset in embryonic conditional knockout heart, we identified a class of the master cardiac regulator GATA4 bound enhancers. With combinatorial assembly of chromatin signatures, we further refined that a unique type of fetal distal GATA4 enhancers enriched for H3K27ac, H3K4me1, but not for H3K4me3 and RNA polymerase II, are reinstated in adult hypertrophic heart. Study Gata4 and histone modifications in E12.5, Adult, Banding and Sham, and to correlate to gene expression and heart function
2014-08-13 | E-GEOD-52123 | biostudies-arrayexpress
Project description:Background: Cardiac transcription factors are master regulators during heart development. Recently, some were shown to transdifferentiate noncardiac mesoderm cells and cardiac fibroblasts into cardiomyocytes. However, the individual roles of each transcription factors in activating cardiac gene program have not been elucidated. We examined cardiac-specific and genome-wide gene expression in fibroblasts induced with cardiac transcription factors Nkx2.5 (N), Tbx5 (T), Gata4 (G), Myocardin (M) alone or different combinations. Methodology/Principal Findings: We applied different combinations of human Nkx2.5 (N), Tbx5 (T), Gata4 (G) and Myocardin (M) lentiviruses into 10T1/2 fibroblasts. Immunostaining and quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed that N, T, G or M alone did not induce expression of cardiac marker genes M-NM-1-myosin heavy chain (M-NM-1MHC) and cardiac troponin T (cTnT). Only T+M and T+G+M combinations induced M-NM-1MHC and cTnT expression. Microarray-based gene ontology analysis revealed that T alone inhibited most genes involved in cardiac-related processes and activated genes involved in Wnt receptor signaling pathway and in aberrant processes. M alone inhibited genes involved in Wnt receptor signaling pathway and activated genes involved in cardiac-related processes and in aberrant processes. G alone inhibited genes involved in ectoderm development. T+G+M combination was the most effective activator of genes associated with cardiac-related processes including muscle cell differentiation, sarcomere, striated muscle contraction, regulation of heart contraction, and glucose metabolism and fatty acid oxidation (two significant forms of cardiomyocyte energy metabolism). And unlike T, M, G alone or T+M, T+G+M did not activate genes associated with aberrant processes. Conclusions: Tbx5, Gata4 and Myocardin play different roles in activating cardiac gene program and in avoiding aberrant gene program activation. The combination of T+G+M activated cardiac gene program and avoided aberrant gene program activation. Two weeks after doxycline induction, total RNA was isolated from 10T1/2-tTA cells infected with different combinations of Tbx5, Gata4, and Myocardin lentiviruses. Biological triplicated.
2012-11-30 | E-GEOD-27329 | biostudies-arrayexpress
Project description:Fibroblasts from different anatomical origins exhibit distinct phenotypic properties. In this study, we aimed to determine the cell-type-specific transcriptional responses to GATA4 overexpression. We performed bulk RNA-seq on cardiac fibroblasts (CF), lung fibroblasts (LF), and tail tip fibroblasts (TTF) transduced with either Ad-GFP (control) or Ad-Cre (GATA4 KO). The goal is to delineate the general versus source-specific GATA4 regulatory networks.
2026-07-01 | GSE325933 | GEO
Project description:Through integration of GATA4 genome-wide occupancy and RNA-seq dataset in embryonic conditional knockout heart, we identified a class of the master cardiac regulator GATA4 bound enhancers. With combinatorial assembly of chromatin signatures, we further refined that a unique type of fetal distal GATA4 enhancers enriched for H3K27ac, H3K4me1, but not for H3K4me3 and RNA polymerase II, are reinstated in adult hypertrophic heart.
2014-08-13 | GSE52123 | GEO
Project description:An important event in the pathogenesis of heart failure is the development of pathological cardiac hypertrophy. In cultured cardiac cardiomyocytes, the transcription factor Gata4 is required for agonist-induced cardiomyocyte hypertrophy. We hypothesized that in the intact organism Gata4 is an important regulator of postnatal heart function and of the hypertrophic response of the heart to pathological stress. To test this hypothesis, we studied mice heterozygous for deletion of the second exon of Gata4 (G4D). At baseline, G4D mice had mild systolic and diastolic dysfunction associated with reduced heart weight and decreased cardiomyocyte number. After transverse aortic constriction (TAC), G4D mice developed overt heart failure and eccentric cardiac hypertrophy, associated with significantly increased fibrosis and cardiomyocyte apoptosis. Inhibition of apoptosis by overexpression of the insulin-like growth factor 1 receptor prevented TAC-induced heart failure in G4D mice. Unlike WT-TAC controls, G4D-TAC cardiomyocytes hypertrophied by increasing in length more than width. Gene expression profiling revealed upregulation of genes associated with apoptosis and fibrosis, including members of the TGF? pathway. Our data demonstrate that Gata4 is essential for cardiac function in the postnatal heart. After pressure overload, Gata4 regulates the pattern of cardiomyocyte hypertrophy and protects the heart from load-induced failure. Keywords: genetic modification, pressure overload stress response
2006-08-12 | GSE5500 | GEO
Project description:The transcription factors MEF2C, GATA4, and TBX5 (MGT) are well established for converting fibroblasts into induced cardiomyocytes (iCMs). However, these reprogramming factors contain effector domains, yet their functional roles in cardiac reprogramming remain largely uncharacterized. Furthermore, whether internal deletions of these domains improve or compromise reprogramming efficiency has not been elucidated. Here we found that the combination of MEF2C and GATA4 mutants (MΔGΔT) elevated reprogramming efficiency by 7-fold to ~21%, achieving robust induction of iCMs with well-defined sarcomeric structures.
2025-06-30 | GSE300140 | GEO