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LncRNA expression profiling of the early mesoderm reveals LncCPR as a novel regulator of cardiogenesis in mice

ABSTRACT: Whole mount in situ hybridization analysis of the 17 lncRNAs revealed that lncRNAs 2410006H16Rik and 4930500J02Rik were expressed in mouse hearts at E9.5. 4930500J02Rik, renamed Long Noncoding Cardiac-promoting RNA (LncCPR), was also enriched in postnatal and adult heart tissue. We hypothesized that the loss of LncCPR expression would directly affect cardiogenesis. To test this hypothesis, we performed functional studies of ESC differentiation after knocking out the LncCPR gene with the CRISPR/Cas9 system. We profiled the transcriptome of mouse ES cells after the loss of LncCPR expression. We found the downregulation of Mesp1 and cardiac transcription factors, as well as a significant reduction in contractility and levels of cardiac structural protein TNNT2. Our findings indicate that LncCPR is a novel, specific regulator of Mesp1, and therefore, of early cardiogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE79499 | GEO | 2019/03/21

REPOSITORIES: GEO

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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.

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LncRNA expression profiling of the early mesoderm reveals LncCPR as a novel regulator of cardiogenesis in mice

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