Quantitative Analysis of Cardiomyocyte-specific Tbx20 Overexpression and Control Mouse Heart Transcriptomes Using Next Generation Sequencing
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE72699 | GEO | 2018/09/02
REPOSITORIES: GEO
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Project description:The goal of this study is to understand the function of cardiac tbx20 during heart regeneration. By high-throughput sequencing, molecular variations of tbx20-cardiac specific inducing heart in response to heart injury compared with control hearts were demonstrated. We collected the injured heart apex tissue at 7 days post injury and sequenced the transcriptome.
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Project description:Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM. Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM.
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Project description:Tbx20 is a transcription factor known to play important roles in embryonic and adult mouse heart function. Our goal in this work was to better understand the function of this gene in embryonic (E11.5) mouse cardiomyocytes that form the developing chambers, expanding our knowledge of its role in heart development. To elucidate the role of Tbx20 in mouse cardiomyocytes, we generated conditional Tbx20 knockout and compared 4 samples with 4 samples of wild-type cardiomyocytes. We found evidence of regulation of cell cycle genes by Tbx20, which are involved in proliferation. In addition, Tbx20 seems to bind and regulate an enhancer of CoupTFII in the atrium, a gene involved in atrial development.
2018-06-14 | E-MTAB-5596 | biostudies-arrayexpress
Project description:To investigate roles for Tbx20 in endocardium, we ablated Tbx20 utilizing Tie2Cre. Tie2Cre;Tbx20 mutants died at E14, exhibiting defects in multiple aspects of cardiac septation. Although endocardial cells lacking Tbx20 were able to undergo endothelial-to-mesenchymal transition, cushion mesenchymal cells lacking Tbx20 did not disperse normally. Non-cell autonomous roles of endocardial Tbx20 were also revealed, as evidenced by decreased myocardialization of outflow tract and failure of dorsal mesenchymal protrusion formation in mutants. To examine how ablation of Tbx20 in endocardial lineages affected gene expression, we performed global gene expression analysis on purified endocardial lineages. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). Mutant endocardial lineages exhibited decreased expression of genes associated with extracellular matrix and cell migration. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). FACS sorted Tie2Cre lineage from E12.5 hearts: Tie2Cre;Tbx20 +/loxP Control hearts versus Tie2Cre;Tbx20 loxP/- mutant hearts
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Project description:To investigate roles for Tbx20 in endocardium, we ablated Tbx20 utilizing Tie2Cre. Tie2Cre;Tbx20 mutants died at E14, exhibiting defects in multiple aspects of cardiac septation. Although endocardial cells lacking Tbx20 were able to undergo endothelial-to-mesenchymal transition, cushion mesenchymal cells lacking Tbx20 did not disperse normally. Non-cell autonomous roles of endocardial Tbx20 were also revealed, as evidenced by decreased myocardialization of outflow tract and failure of dorsal mesenchymal protrusion formation in mutants. To examine how ablation of Tbx20 in endocardial lineages affected gene expression, we performed global gene expression analysis on purified endocardial lineages. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). Mutant endocardial lineages exhibited decreased expression of genes associated with extracellular matrix and cell migration. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+).
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Project description:Tbx20 is a transcription factor important for heart development. To assess the role of Tbx20 in the adult heart, we sought to identify regulatory regions, gene targets and pathways regulated by this TF. To this end, we used chromatin immunoprecipitation (ChIP) of Tbx20 fused to GFP to locate binding sites in the genome of 8 weeks whole heart mouse tissue.
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Project description:Tbx20 is a transcription factor important for heart development. To assess the role of Tbx20 in the adult heart, we sought to identify regulatory regions, gene targets and pathways regulated by this TF. To this end, we used chromatin immunoprecipitation (ChIP) of Tbx20 fused to GFP to locate binding sites in the genome of 8 weeks whole heart mouse tissue. Analysis of 1 Tbx20-GFP ChIP sample of adult mouse whole heart against whole heart input
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Project description:Tbx20 is a transcription factor important for heart development. To assess the role of Tbx20 in the adult heart, we generated a conditional knockout for this gene, specifically in cardiomyocytes. We profiled gene expression levels using RNA-seq in both normal and knockout adult mouse hearts to identify genes and pathways regulated by Tbx20. The article describing the Tbx20 knockout mouse is under review, a reference will be added when published.
2012-02-10 | GSE30943 | GEO
Project description:T-box transcription factor 20 (Tbx20) plays a multifaceted role in cardiac morphogenesis and controls a broad gene regulatory network. However, the mechanism by which Tbx20 activates and represses target genes in a tissue-specific and temporal manner remains unclear. Studies show that Tbx20 directly interacts with the Transducin-like Enhancer of Split (TLE) family of proteins to mediate transcriptional repression. However, a function for the Tbx20-TLE transcriptional repression complex during heart development has yet to be established. We created a mouse model with a two-amino acid substitution in the Tbx20 EH1 domain, thereby disrupting the Tbx20-TLE interaction. Disruption of this interaction impaired critical morphogenic events, including cardiac looping and chamber formation. Transcriptional profiling of Tbx20EH1Mut hearts and analysis of putative direct targets revealed misexpression of the retinoic acid pathway and cardiac progenitor genes. Further, we show that altered cardiac progenitor development and function contribute to the severe cardiac defects in our model. Our studies indicate that TLE-mediated repression is a primary mechanism by which Tbx20 controls gene expression.
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Project description:We performed ChIP-seq of Tbx20 tagged with GFP in mouse hearts to identify binding sites for this transcription factor. This data set is part of the study âEndocardial Tbx20 is essential for mesenchymal and myocardial cell movements required for cardiac septationâ.
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