Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin; germline Parkin knockout mouse hearts

Dysfunctional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathological process underlying Parkinson disease and a potential genetic mechanism of cardiomyopathy. Despite epidemiological associations between Parkinson disease and heart failure, the role of Parkin and mitophagic quality control in maintaining normal cardiac homeostasis is poorly understood.We used germline mutants and cardiac-specific RNA interference to interrogate Parkin regulation of cardiomyocyte mitochondria and examine functional crosstalk between mitophagy and mitochondrial dynamics in Drosophila heart tubes. 5 wild-type mouse hearts; 4 germline Parkin knockout mouse hearts Please note that the mouse cardiac examples were an adjunct to the Drosophila studies that comprised most of the associated publication. However, mRNA-sequencing was only performed on the mouse samples, not the Drosophila heart tubes.功能失调的帕金蛋白（Parkin）介导的线粒体自噬清除衰老或受损线粒体的过程，是帕金森病的主要病理过程，同时也是心肌病的潜在遗传机制。尽管帕金森病与心力衰竭之间已被证实存在流行病学关联，但学界对帕金蛋白及线粒体自噬质量控制在维持正常心脏稳态中的作用仍知之甚少。本研究借助生殖系突变体与心脏特异性RNA干扰（RNA interference）技术，在果蝇心管中探究帕金蛋白对心肌细胞线粒体的调控作用，并解析线粒体自噬与线粒体动力学之间的功能性互作。实验样本包括5只野生型小鼠心脏与4只生殖系帕金基因敲除（Parkin knockout）小鼠心脏。请注意，小鼠心脏样本仅作为果蝇研究的辅助实验对象，后者构成了相关发表论文的主体内容。然而，仅对小鼠样本开展了mRNA测序（mRNA-sequencing），未对果蝇心管进行此项实验。