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Temporal Quantitative Proteomic Profiling of Murine Embryonic Heart Development

ABSTRACT: Comprehensive detail of the molecular mechanisms that govern heart development is essential for identifying the etiology of congenital heart disease. We used high-throughput quantitative proteomics to measure temporal changes in the cardiac proteome at eight critical stages of murine embryonic heart development. We identified more than 7,300 proteins, assessed global temporal changes in protein expression, identified cardiac protein interaction networks, and linked protein dynamics with molecular pathways. Using this dataset, we identified and defined a function for the mevalonate pathway in the regulation of embryonic cardiomyocyte proliferation and cell signaling. Overall, our proteomic datasets are an invaluable resource for studying molecular events that regulate embryonic heart development and that contribute to congenital heart disease.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Laura Herring

LAB HEAD: Frank Conlon

PROVIDER: PXD032312 | Pride | 2023-04-06

REPOSITORIES: Pride

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			Action	DRS
	20200618_Lumos_PC691-Conlon-Set1_F1-test.raw	Raw
	20200618_Lumos_PC691-Conlon-Set1_F10.raw	Raw
	20200618_Lumos_PC691-Conlon-Set1_F11.raw	Raw
	20200618_Lumos_PC691-Conlon-Set1_F12.raw	Raw
	20200618_Lumos_PC691-Conlon-Set1_F13.raw	Raw

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Project description:Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease. To interrogate the temporal and spatial expression profiles across the entire genome during mammalian heart development, we designed a time-course microarray experiment using the mouse model at defined stages of cardiogenesis, starting with embryonic stem cells (ESC, R1 stem cell line), early embryonic developmental stages: E7.5 whole embryos, E8.5 heart tubes, left and right ventricle tissues at E9.5, E12.5, E14.5, E18.5 to 3 days after birth (D3) and adult heart (Figure 1A). At each time point, microarray experiments were performed on triplicate biological samples. Starting at E9.5, tissue samples from left ventricles (LV) and right ventricles (RV) were microdissected for RNA purification and microarray analysis to determine spatially differential gene expression between LV and RV during heart development.

Dataset Information

Temporal Quantitative Proteomic Profiling of Murine Embryonic Heart Development

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