The ubiquitin ligase Mul1 induces mitophagy in skeletal muscle in response to muscle-wasting stimuli
- PMID: 23140641
- DOI: 10.1016/j.cmet.2012.10.005
The ubiquitin ligase Mul1 induces mitophagy in skeletal muscle in response to muscle-wasting stimuli
Retraction in
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Retraction Notice to: The Ubiquitin Ligase Mul1 Induces Mitophagy in Skeletal Muscle in Response to Muscle-Wasting Stimuli.Cell Metab. 2015 Dec 1;22(6):1090. doi: 10.1016/j.cmet.2015.11.010. Cell Metab. 2015. PMID: 26973995
Abstract
Recent research reveals that dysfunction and subsequent loss of mitochondria (mitophagy) is a potent inducer of skeletal muscle wasting. However, the molecular mechanisms that govern the deregulation of mitochondrial function during muscle wasting are unclear. In this report, we show that different muscle-wasting stimuli upregulated mitochondrial E3 ubiquitin protein ligase 1 (Mul1), through a mechanism involving FoxO1/3 transcription factors. Overexpression of Mul1 in skeletal muscles and myoblast cultures was sufficient for the induction of mitophagy. Consistently, Mul1 suppression not only protected against mitophagy but also partially rescued the muscle wasting observed in response to muscle-wasting stimuli. In addition, upregulation of Mul1, while increasing mitochondrial fission, resulted in ubiquitination and degradation of the mitochondrial fusion protein Mfn2. Collectively, these data explain the molecular basis for the loss of mitochondrial number during muscle wasting.
Copyright © 2012 Elsevier Inc. All rights reserved.
Comment in
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The missing link: Mul1 signals mitophagy and muscle wasting.Cell Metab. 2012 Nov 7;16(5):551-2. doi: 10.1016/j.cmet.2012.10.013. Cell Metab. 2012. PMID: 23140636
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