PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (Spatial Transcriptomics)
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Summary:
The loss of compact myocardial cardiomyocyte (compact CM) identity suggests that PRDM16 deficiency may dramatically alter the cellular composition in left ventricular (LV) compact myocardium. To test this hypothesis, we performed single-cell RNA-seq (scRNA-seq) to examine gene dysreulation in Prdm16cKO heart. We also performed Visium Spatial Transcriptomics (ST) to facilitate mapping CM clusters to their original locations in the heart. As a result, we were able to demonstrate gene misregulation in Prdm16cKO mouse mainly occurred in LV compact CM.Overall design:
Two pairs of Prdm16cKO/WT E13.5 mouse hearts and two pairs of Prdm16cKO/control E15.5 mouse hearts were used for Visium Spatial Transcriptomics (ST).Technology:
10x Visium
Platform:
Illumina NovaSeq 6000
Species:
Mus musculus(mm10)
Tissues:
Heart
Development stage:
E13.5, E15.5
Citation:
Wu, Tongbin et al. “PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle.” Circulation vol. 145,8 (2022): 586-602. doi:10.1161/CIRCULATIONAHA.121.056666Submission date: 2021-07-03Update date: 2021-12-21
Sample number: 4
Contributors
Tongbin Wu; Zhengyu Liang; Ju Chen
Contact: juchen@health.ucsd.edu