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The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

ABSTRACT: In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample.

ORGANISM(S): Mus musculus

PROVIDER: GSE14906 | GEO | 2010/02/18

SECONDARY ACCESSION(S): PRJNA112009

REPOSITORIES: GEO

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The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

Project description:In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample. We have analyzed 6 RNA samples total (3 from control hearts, 2 from FOG2 null hearts and 1 from GATA4ki hearts)

2010-02-21 | E-GEOD-14906 | biostudies-arrayexpress

Transcription profiling of mouse Gata4ki/ki ovaries reveals ovarian development in mice requires GATA4/FOG2 transcriptional complex

Project description:We have demonstrated previously that mammalian sexual differentiation requires both GATA4 and FOG2 transcription regulators to assemble the functioning testis. We have now determined that the sexual development of female mice is profoundly affected by the loss of GATA4-FOG2 interaction. We have also identified the Dkk1 gene, encoding a secreted inhibitor of canonical Î²-catenin signaling as a target of GATA4/FOG2 repression in the developing ovary. The tissue-specific ablation of the Î²-catenin gene in the gonads disrupts female development while in the Gata4ki/ki/Dkk1-/- or Fog2-/-/Dkk1-/- embryos the normal ovarian gene expression pattern is partially restored. Control of ovarian development by the GATA4/FOG2 complex presents a novel insight into the crosstalk of transcriptional regulation and extracellular signaling in ovarian development. Experiment Overall Design: 6 control and 6 Gata4ki/ki mutant samples were analyzed

2009-05-11 | E-GEOD-11314 | biostudies-arrayexpress

Ovarian Development in Mice Requires GATA4/FOG2 Transcriptional Complex

Project description:We have demonstrated previously that mammalian sexual differentiation requires both GATA4 and FOG2 transcription regulators to assemble the functioning testis. We have now determined that the sexual development of female mice is profoundly affected by the loss of GATA4-FOG2 interaction. We have also identified the Dkk1 gene, encoding a secreted inhibitor of canonical β-catenin signaling as a target of GATA4/FOG2 repression in the developing ovary. The tissue-specific ablation of the β-catenin gene in the gonads disrupts female development while in the Gata4ki/ki/Dkk1-/- or Fog2-/-/Dkk1-/- embryos the normal ovarian gene expression pattern is partially restored. Control of ovarian development by the GATA4/FOG2 complex presents a novel insight into the crosstalk of transcriptional regulation and extracellular signaling in ovarian development. Keywords: genetic modification

2009-05-01 | GSE11314 | GEO

Fog2 regulation of gene expression in the adult heart

Project description:MHCaCre induced knockout of Fog2flox. Aberrant transcriptional regulation contributes to the pathogenesis of both congenital and adult forms of heart disease. While the transcriptional regulator FOG2 is known to be essential for heart morphogenesis and coronary development, its tissue specific function has not been previously investigated. Additionally, little is known about the role of FOG2 in the adult heart. Here we use spatiotemporally regulated inactivation of Fog2 to delineate its function both in embryo and adult heart. Early cardiomyocyte-restricted loss of Fog2 recapitulated the cardiac and coronary defects of the Fog2 germline knockouts. Later cardiomyocyte-restricted loss of Fog2 (Fog2MC) did not result in defects in cardiac structure or coronary vessel formation. However, Fog2MC adult mice had severely depressed ventricular function and died at 8-14 weeks. Fog2MC adult hearts displayed a paucity of coronary vessels. This was associated with myocardial hypoxia, increased cardiomyocyte apoptosis, and cardiac fibrosis. Induced inactivation of Fog2 in adult heart resulted in similar phenotype, as did ablation of FOG2 interaction with the transcription factor GATA4. Loss of FOG2 or FOG2-GATA4 interaction altered expression of a panel of angiogenesis-related genes. Collectively, our data indicated that FOG2 regulates adult heart function and coronary angiogenesis.

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Transcription profiling of mouse Fog2flox/delta; MHCaCre vs. Fog2flox/deltaFog2 to investigate Fog2 regulation of gene expression in the adult heart

2009-03-15 | E-GEOD-15078 | biostudies-arrayexpress

Mus musculus

Project description:The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

| PRJNA112009 | ENA

FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ncRNA-Seq]

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [ChIP-Seq]

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FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk [RNA-Seq]

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Gene expression profiling of E12.5 wildtype- and Sp3 null hearts

Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Keywords: Transcription factors, Sp3, knockout mice, cardiac malformations, E12.5

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