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ChIP-seq of Tbx20 tagged with GFP in E11.5 mouse hearts

ABSTRACT: ChIP-seq of Tbx20 tagged with GFP in E11.5 mouse hearts

PROVIDER: PRJEB11457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1079228.fastq.gz	Fastqsanger.gz
	ERR1079229.fastq.gz	Fastqsanger.gz

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ChIP-seq of Tbx20 tagged with GFP in E11.5 mouse hearts

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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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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