The Organization of Mitochondrial Quality Control and Life Cycle in the Nervous System In Vivo in the Absence of PINK1.

摘要: Maintenance of healthy mitochondria is crucial in cells, such as neurons, with high metabolic demands, and dysfunctional are thought to be selectively degraded. Studies chemically uncoupled cells have implicated PINK1 mitochondrial kinase, Parkin E3 ubiquitin ligase targeting depolarized for degradation. However, the role PINK1/Parkin pathway turnover unclear nervous system under normal physiological conditions, we understand little about changes that occur life cycle when disrupted. Here, evaluated nature, location, regulation quality control vivo using quantitative measurements Drosophila system, deletion overexpression genes pathway. We tested hypotheses impairment via suppression function should produce failures turnover, accumulation senescent axon, defects traffic, a significant shift fission–fusion steady state. Although membrane potential was diminished by deletion, did not observe predicted increases density or length axons. Loss also produced specific, directionally balanced transport, without altering balance between stationary moving mitochondria. Somatic morphology compromised. These results strongly circumscribe possible mechanisms action raise possibility events cultured embryonic axons might restricted cell body vivo, intact system.