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Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy
Journal article   Open access   Peer reviewed

Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy

Rhianna C Laker, Joshua C Drake, Rebecca J Wilson, Vitor A Lira, Bevan M Lewellen, Karen A Ryall, Carleigh C Fisher, Mei Zhang, Jeffrey J Saucerman, Laurie J Goodyear, …
Nature communications, Vol.8(1), 548
09/15/2017
DOI: 10.1038/s41467-017-00520-9
PMCID: PMC5601463
PMID: 28916822
url
https://doi.org/10.1038/s41467-017-00520-9View
Published (Version of record) Open Access

Abstract

Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555. Using mice expressing dominant negative and constitutively active Ampk in skeletal muscle, we demonstrate that Ulk1 activation is dependent on Ampk. Furthermore, exercise-induced metabolic adaptation requires Ulk1. These findings provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 signaling in skeletal muscle.Exercise is associated with biogenesis and removal of dysfunctional mitochondria. Here the authors use a mitochondrial reporter gene to demonstrate the occurrence of mitophagy following exercise in mice, and show this is dependent on AMPK and ULK1 signaling.
Exercise Oxidative Stress Phosphorylation Amino Acid Motifs AMP-Activated Protein Kinases - chemistry AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism Animals Autophagy-Related Protein-1 Homolog - chemistry Autophagy-Related Protein-1 Homolog - genetics Autophagy-Related Protein-1 Homolog - metabolism Humans Lysosomes - enzymology Lysosomes - genetics Male Mice Mice, Inbred C57BL Mitochondria - enzymology Mitochondria - genetics Mitophagy Muscle, Skeletal - enzymology Muscle, Skeletal - metabolism

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