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Abstract
PINK1, mutated in familial forms of Parkinson’s disease, initiates mitophagy following mitochondrial depolarization. However, it is difficult to monitor this pathway physiologically in mice as loss of PINK1 does not alter basal mitophagy levels in most tissues. To further characterize this pathway in vivo, we used mito-QC mice in which loss of PINK1 was combined with the mitochondrial-associated POLGD257A mutation. We focused on skeletal muscle as gene expression data indicates that this tissue has the highest PINK1 levels. We found that loss of PINK1 in oxidative hindlimb muscle significantly reduced mitophagy. Of interest, the presence of the POLGD257A mutation, while having a minor effect in most tissues, restored levels of muscle mitophagy caused by the loss of PINK1. Although our observations highlight that multiple mitophagy pathways operate within a single tissue, we identify skeletal muscle as a tissue of choice for the study of PINK1-dependant mitophagy under basal conditions.
Original language | English |
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Article number | 2326402 |
Number of pages | 19 |
Journal | Autophagy Reports |
Volume | 3 |
Issue number | 1 |
Early online date | 11 Mar 2024 |
DOIs | |
Publication status | Published - 2024 |
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Dive into the research topics of 'PINK1 regulated mitophagy is evident in skeletal muscles'. Together they form a unique fingerprint.Projects
- 1 Finished
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Advancing Tissue Imaging Capabilities with Airyscan Confocal Microscopy (Multiuser Equipment Grant)
Ganley, I. (Investigator), Januschke, J. (Investigator), Muqit, M. (Investigator), Storey, K. (Investigator), Swedlow, J. (Investigator) & Tanaka, T. (Investigator)
26/09/17 → 1/01/19
Project: Research