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Temporal multiomics gene expression data across human embryonic stem cell derived cardiomyocyte differentiation

ABSTRACT: Embryonic development has not been fully understood, despite significant advances in molecular and systems-level approaches. Human embryonic stem cells (hESCs) serve as a valuable in vitro model for studying early human developmental processes due to their ability to differentiate into all three germ layers. Here, we present a comprehensive multi-omics dataset generated by differentiating hESCs into cardiomyocytes via the mesodermal lineage, collecting samples at 10 distinct time points. We measured mRNA levels by mRNA sequencing (mRNA-seq), translation levels by ribosome profiling (Ribo-seq), and protein levels by quantitative mass spectrometry. Technical validation confirmed high quality and reproducibility across all datasets, with strong correlations between replicates. This extensive dataset provides critical insights into the complex regulatory mechanisms of cardiomyocyte differentiation and serves as a valuable resource for the research community, aiding in the exploration of mammalian development and gene regulation.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Marko Jovanovic

PROVIDER: MSV000095595 | MassIVE | Wed Aug 14 00:54:00 BST 2024

REPOSITORIES: MassIVE

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Project description:Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. These microRNAs (miRs) are expressed during early stages of heart development, and they regulate a highly complex gene regulatory network (GRN). To study the in vivo and in vitro function of specific miR-200 family members we inhibited individual members of the miR-200 family during embryonic development. Inhibition of a single miR-200 family member within the cluster caused defects in the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family resulted in a ventral septal defect and embryonic lethality by embryonic day (E)16.5. In cardiomyocytes, the miR-200 family targets the transcripts of Tbx5, Gata4, Mef2c and Pitx2. Inhibition of this family increased expression of Tbx5, Gata4, Mef2c and Pitx2 in both the left ventricle and atria across multiple stages of cardiac development. Embryos with reduced levels of a single miR-200 family member were non-lethal and pups survived into adulthood. At postnatal day (P) 1 these pups had a reduced heart rate and increased ventricular wall thickness. Each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing revealed a new cardiomyocyte cell state, suggesting these cells were less differentiated due to inhibition of the miR-200 family. We have identified several new transcription factors regulated by miR-200 during heart development. The miR-200 family are critical regulators of early cardiac development through maintaining gene dosage of Tbx5, Gata4, Mef2c and Pitx2, which affects cardiomyocyte differentiation and maturation. The multiomics analyses of early heart development after miR-200 inhibition reveals a new cardiomyocyte less differentiated cell state and chromatin modifications due to the function of the miR-200 family.

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Temporal multiomics gene expression data across human embryonic stem cell derived cardiomyocyte differentiation

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