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In skeletal muscle, ethanol causes alcoholic myopathy, which is characterized by myofiber atrophy and the loss of muscle strength. Alcoholic myopathy is more prevalent than all inherited muscle diseases combined. Current evidence indicates that ethanol directly impairs muscle organization and function. However, the underlying mechanism by which ethanol causes toxicity in muscle is poorly understood. Here, we show that the nematode\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    exhibits the key features of alcoholic myopathy when exposed to ethanol. As in mammals, ethanol exposure impairs muscle strength and induces the expression of protective genes, including oxidative stress response genes. In addition, ethanol exposure causes the fragmentation of mitochondrial networks aligned with myofibril lattices. This ethanol\u2010induced mitochondrial fragmentation is dependent on the mitochondrial fission factor DRP\u20101 (dynamin\u2010related protein 1) and its receptor proteins on the outer mitochondrial membrane. Our data indicate that this fragmentation contributes to the activation of the mitochondrial unfolded protein response (UPR). We also found that robust, perpetual mitochondrial UPR activation effectively reduces muscle weakness caused by ethanol exposure. Our results strongly suggest that the modulation of mitochondrial stress responses may provide a method to ameliorate alcohol toxicity and damage to muscle.\n                  <\/jats:p>","DOI":"10.1096\/fj.201903166r","type":"journal-article","created":{"date-parts":[[2020,4,15]],"date-time":"2020-04-15T12:18:28Z","timestamp":1586953108000},"page":"8204-8216","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Alcohol induces mitochondrial fragmentation and stress responses to maintain normal muscle function in\n                    <i>Caenorhabditis elegans<\/i>"],"prefix":"10.1096","volume":"34","author":[{"given":"Kelly H.","family":"Oh","sequence":"first","affiliation":[{"name":"Department of Cell Biology &amp; Anatomy Center for Cancer Cell Biology, Immunology, and Infection Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago IL USA"},{"name":"School of Graduate and Postdoctoral Studies Rosalind Franklin University of Medicine and Science North Chicago IL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seema","family":"Sheoran","sequence":"additional","affiliation":[{"name":"Department of Biological Science University of Illinois at Chicago Chicago IL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet E.","family":"Richmond","sequence":"additional","affiliation":[{"name":"Department of Biological Science University of Illinois at Chicago Chicago IL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongkyun","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Cell Biology &amp; Anatomy Center for Cancer Cell Biology, Immunology, and Infection Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago IL USA"},{"name":"School of Graduate and Postdoctoral Studies Rosalind Franklin University of Medicine and Science North Chicago IL 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