Abstract
Cardiac myocyte-specific gene manipulation is facilitated by reagents permitting temporal control over transgene expression or gene ablation, and by physiological phenotyping platforms that complement post-mortem cellular and pathological analyses. The ease of creating cardiac-specific gene modified mice may have contributed to genetic mouse models lacking strong underlying mechanistic rationales; this was argued for genetic ablation of mitochondrial dynamics factors in cardiac myocytes that exhibit little evidence for mitochondrial dynamism. Here, I review recent published studies in which experimental in vivo manipulation of mitochondrial fusion and fission genes has revealed non-canonical functioning dynamics factors in mitochondrial quality and quantity control. Targeting mitochondrial dynamics proteins in the cardiac system, where mitochondrial dynamism is barely observed, was essential to uncovering novel functioning of these factors in other pathways.