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The <mitochondrial fission-fusion cycle> is continuous remodeling of a mitochondrial population by division and merger. In mammalian <biological cells>, <mitofusins> promote fusion of outer mitochondrial membranes, while <OPA1> supports fusion of inner mitochondrial membranes. Fusion mixes matrix contents and permits functional complementation between <mitochondria>. Genetic disruption and rescue of <mitofusins> demonstrated their requirement for normal mitochondrial fusion.<Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development by Hsiuchen Chen and others>[Abstract and Results: mitofusin loss, fragmented mitochondria and rescue]{ref}
For fission, recruited <Drp1> assembles at constrictions and uses <GTP>-dependent remodeling to help divide the <organelle>.<Dynamin-related protein Drp1 is required for mitochondrial division in mammalian cells by Elena Smirnova and others>[Abstract and Results: Drp1 recruitment and division defects]{ref} \b[The balance controls network shape, distribution and quality control.] Division can help distribute <mitochondria> to daughter <biological cells> and segregate damaged portions for <mitophagy>; fusion can restore mixed contents. These are regulated competing events in a network, not an obligatory synchronized sequence that every <mitochondrion> completes on a fixed timetable.
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