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Using transmission electron microscopy, we identified morphological abnormalities in both the mitochondria and the sarcoplasmic reticulum (SR) in aged muscle\u2010specific \u03b2<jats:sub>cyto<\/jats:sub>\u2010 and \u03b3<jats:sub>cyto<\/jats:sub>\u2010actin KO mice. We found \u03b2<jats:sub>cyto<\/jats:sub>\u2010 and \u03b3<jats:sub>cyto<\/jats:sub>\u2010actin proteins to be enriched in isolated mitochondrial\u2010associated membrane preparations, which represent the interface between mitochondria and sarco\u2010endoplasmic reticulum important in signaling and mitochondrial dynamics. We also measured significantly elongated and interconnected mitochondrial morphologies associated with a significant decrease in mitochondrial fission events in primary mouse embryonic fibroblasts lacking \u03b2<jats:sub>cyto<\/jats:sub>\u2010 and\/or \u03b3<jats:sub>cyto<\/jats:sub>\u2010actin. Interestingly, mitochondrial respiration in muscle was not measurably affected as oxygen consumption was similar in skeletal muscle fibers from 12\u00a0month\u2010old muscle\u2010specific \u03b2<jats:sub>cyto<\/jats:sub>\u2010 and \u03b3<jats:sub>cyto<\/jats:sub>\u2010actin KO mice. Instead, we found that the maximal rate of relaxation after isometric contraction was significantly slowed in muscles of 12\u2010month\u2010old \u03b2<jats:sub>cyto<\/jats:sub>\u2010 and \u03b3<jats:sub>cyto<\/jats:sub>\u2010actin muscle\u2010specific KO mice. Our data suggest that impaired Ca<jats:sup>2+<\/jats:sup> re\u2010uptake may presage development of the observed <jats:styled-content style=\"fixed-case\">SR<\/jats:styled-content> morphological changes in aged mice while providing a potential pathological mechanism for the observed myopathy.<\/jats:p>","DOI":"10.1111\/febs.14367","type":"journal-article","created":{"date-parts":[[2017,12,19]],"date-time":"2017-12-19T03:22:43Z","timestamp":1513653763000},"page":"481-500","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Impaired muscle relaxation and mitochondrial fission associated with genetic ablation of cytoplasmic actin isoforms"],"prefix":"10.1111","volume":"285","author":[{"given":"Allison R.","family":"O'Rourke","sequence":"first","affiliation":[{"name":"Department of Genetics, Cell Biology and Development University of Minnesota Minneapolis MN 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