PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (Spatial Transcriptomics)

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. 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).致密层心肌细胞（compact myocardial cardiomyocyte, compact CM）的身份丧失提示，PRDM16缺失可能会显著改变左心室（left ventricular, LV）致密层心肌的细胞组成。为验证这一假说，我们通过单细胞RNA测序（single-cell RNA-seq, scRNA-seq）检测了Prdm16cKO心脏中的基因表达失调情况。此外，我们还开展了Visium空间转录组学（Visium Spatial Transcriptomics, ST），以辅助将心肌细胞簇映射至其在心脏内的原始位置。最终，我们证实Prdm16cKO小鼠的基因失调主要发生于左心室致密层心肌细胞。本研究共使用2组Prdm16cKO/WT E13.5小鼠心脏样本，以及2组Prdm16cKO/对照E15.5小鼠心脏样本用于Visium空间转录组学检测。