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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE198788 | GEO | 2024/05/02

REPOSITORIES: GEO

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

Project description:The transcription factor FOG2 (ZFPM2) is upregulated in human heart failure and increased FOG2 expression causes heart failure in mice. We found that FOG2 directly intersects a gene regulatory network driven by the atrial-enriched TF TBX5 and required for atrial cardiomyocyte rhythm control gene expression

2024-05-02 | GSE198786 | GEO

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

2024-05-02 | GSE198734 | GEO

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

2024-05-02 | GSE198733 | GEO

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

Project description:FOG2 modulates a TBX5/GATA4-co-ocupied atrial gene regulatory network linking heart failure to atrial fibrillation risk

| PRJNA816871 | ENA

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

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

| PRJNA816708 | ENA

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

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

| PRJNA816709 | ENA

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

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

| PRJNA816873 | ENA

An atrial fibrillation-associated regulatory region modulates cardiac <i>Tbx5</i> levels and arrhythmia susceptibility.

Project description:Heart development and rhythm control are highly Tbx5 dosage-sensitive. TBX5 haploinsufficiency causes congenital conduction disorders, whereas increased expression levels of TBX5 in human heart samples has been associated with atrial fibrillation (AF). We deleted the conserved mouse orthologues of two independent AF-associated genomic regions in the Tbx5 locus, one intronic (RE(int)) and one downstream (RE(down)) of Tbx5. In both lines, we observed a modest (30%) increase of Tbx5 in the postnatal atria. To gain insight into the effects of slight dosage increase in vivo, we investigated the atrial transcriptional, epigenetic and electrophysiological properties of both lines. Increased atrial Tbx5 expression was associated with induction of genes involved in development, ion transport and conduction, with increased susceptibility to atrial arrhythmias, and increased action potential duration of atrial cardiomyocytes. We identified an AF-associated variant in the human RE(int) that increases its transcriptional activity. Expression of the AF-associated transcription factor Prrx1 was induced in Tbx5RE(int)KO cardiomyocytes. We found that some of the transcriptional and functional changes in the atria caused by increased Tbx5 expression were normalized when reducing cardiac Prrx1 expression in Tbx5RE(int)KO mice, indicating an interaction between these two AF genes. We conclude that modest increases in expression of dose-dependent transcription factors, caused by common regulatory variants, significantly impact on the cardiac gene regulatory network and disease susceptibility.

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An endocardial pathway involving Tbx5, Gata4, and Nos3 required for atrial septum formation.

Project description:In humans, septal defects are among the most prevalent congenital heart diseases, but their cellular and molecular origins are not fully understood. We report that transcription factor Tbx5 is present in a subpopulation of endocardial cells and that its deletion therein results in fully penetrant, dose-dependent atrial septal defects in mice. Increased apoptosis of endocardial cells lacking Tbx5, as well as neighboring TBX5-positive myocardial cells of the atrial septum through activation of endocardial NOS (Nos3), is the underlying mechanism of disease. Compound Tbx5 and Nos3 haploinsufficiency in mice worsens the cardiac phenotype. The data identify a pathway for endocardial cell survival and unravel a cell-autonomous role for Tbx5 therein. The finding that Nos3, a gene regulated by many congenital heart disease risk factors including stress and diabetes, interacts genetically with Tbx5 provides a molecular framework to understand gene-environment interaction in the setting of human birth defects.

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Art27 interacts with GATA4, FOG2 and NKX2.5 and is a novel co-repressor of cardiac genes.

Project description:Transcription factors play a crucial role in regulation of cardiac biology. FOG-2 is indispensable in this setting, predominantly functioning through a physical interaction with GATA-4. This study aimed to identify novel co-regulators of FOG-2 to further elaborate on its inhibitory activity on GATA-4. The Art27 transcription factor was identified by a yeast-2-hybrid library screen to be a novel FOG-2 protein partner. Characterisation revealed that Art27 is co-expressed with FOG-2 and GATA-4 throughout cardiac myocyte differentiation and in multiple structures of the adult heart. Art27 physically interacts with GATA-4, FOG-2 and other cardiac transcription factors and by this means, down-regulates their activity on cardiac specific promoters α-myosin heavy chain, atrial natriuretic peptide and B-type natriuretic peptide. Regulation of endogenous cardiac genes by Art27 was shown using microarray analysis of P19CL6-Mlc2v-GFP cardiomyocytes. Together these results suggest that Art27 is a novel transcription factor that is involved in downregulation of cardiac specific genes by physically interacting and inhibiting the activity of crucial transcriptions factors involved in cardiac biology.

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