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Mus musculus

ABSTRACT: RNA-sequencing from wild-type (WT) or Tie2-Ino80 knockout (KO) mouse embryo hearts

PROVIDER: PRJNA383935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5468583_1.fastq.gz	Fastqsanger.gz
	SRR5468583_2.fastq.gz	Fastqsanger.gz
	SRR5468584_1.fastq.gz	Fastqsanger.gz
	SRR5468584_2.fastq.gz	Fastqsanger.gz
	SRR5468585_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing from wild-type (WT) or Tie2-Ino80 knockout (KO) mouse embryo hearts

Project description:Purpose: Endothelial cell-specific knockout of the INO80 chromatin-remodeling complex in developing mouse embryos results in defective coronary angiogenesis. Transcriptome analysis on whole hearts was performed to understand how Ino80 regulates the genome to influence angiogenesis. Methods: mRNA was extracted from whole hearts after surgical removal from embryonic day 13.5 mice, either WT or Tie2-Ino80 KO, and prepped for Illumina sequencing using the NEBNext Ultra RNA Library Prep kit. Results: Deletion of Ino80 in the two major coronary progenetiors results in intermediate non-compaction phenotypes and an increase in E2F-mediated gene expression and cellular proliferation. Conclusions: Ino80 normally functions to suppress E2F-mediated proliferation in cardiac endothelial cells in order to promote productive angiogenesis and prevent underdevelopment of the myocardium heart muscle. Loss of this critical chromatin-remodeling function results in human disease phenotypes.

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Mus musculus

Project description:Expression data of E12.5 Slc39a8 knockout (KO) embryo heart and wild type (WT) control

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