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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Cell Metab. 2015 Oct 22;22(6):1033–1044. doi: 10.1016/j.cmet.2015.09.027

Figure 7. Model: the linking of OXPHOS activity and mitochondrial fusion promotes organellar health and restricts spread of mtDNA defects in myofibers.

Figure 7

(Left) In wildtype myofibers, oxidative activity promotes fusion of mitochondria across the sarcomere, thereby promoting some homogenization of the organellar population along the longitudinal axis. Z-lines are depicted in cyan. (Right) In the presence of mutant mtDNA, clonal expansion of the genetic defect (due to unknown mechanisms) results in decreased OXPHOS activity. Decreased OXPHOS at the site of the defect is proposed to lower local fusion rates, thereby promoting compartmentalization and limiting spread of the mutant mtDNA genome throughout the fiber.