Effect of depletion of vacuolar protein sorting 13 homolog c (Vps13c) in heart tissue from ventricles of wild-type (WT) and cardiac-specific knockout (Vps13c-cKO) mice.

Systems genetics strategy across multiple Hybrid Mouse Diversity Panel (HMDP) cohorts pinpointed vacuolar protein sorting 13 homolog c (Vps13c) as a candidate trans-regulator of the mitochondrial transcriptome. Subsequent functional studies revealed that VPS13C influences mitochondrial morphology, bioenergetics, and global gene expression in cardiomyocytes. To assess the in vivo role of Vps13c, we generated Vps13c-flox mice, which were further crossed with Myh6-Cre mice to generate cardiac-specific knockout (Vps13c-cKO) mice. Efficient gene deletion was confirmed by reduced cardiac Vps13c mRNA and protein levels. RNA sequencing of ventricles from WT and Vps13c-cKO mice were performed here to investigate the impact of loss of Vps13c in vivo. RNA seq profiling of ventricles from heart of WT and Vps13c-cKO mice. The experiments were performed at 7 weeks old male mice.