Mitochondrial fusion, fission and autophagy: Impact of diet on mitochondrial quality control

Mitochondrial dynamics and mitophagy are recognized as two critical processes underlying mitochondrial homeostasis. Morphological and bioenergetic characterization of the life cycle of the individual mitochondrion reveals several points where fusion, fission and mitophagy interact. Mitochondrial fission can produce an impaired daughter unit that will be targeted by the autophagic machinery. Mitochondrial fusion, on the other hand may serve to dilute impaired respiratory components and thereby prevent their removal. The reverse dependency of fusion and mitophagy on membrane potential allows them to act as complementary rather than competitive fates of the daughter mitochondrion after a fission event. However, quality control is not the only mitochondrial task that involves changes to mitochondrial architecture. Recent studies of mitochondrial dynamics have identified an intriguing link between energy demand/supply balance and mitochondrial architecture. Cells exposed to rich nutrient environment tend to freeze their architecture at the state of separated (fragmented) mitochondria and cells under starvation tend to stay longer at the connected state. Thus, it appears that bioenergetic adaptation that involves changes to bioenergetic efficiency and ATP synthesis capacity also implies remodeling of mitochondrial architecture. One can appreciate that the life cycle of mitochondria will be compromised if mitochondrial fusion or fission are disabled to allow for bioenergetic adaptation. Therefore bioenergetic adaptation and quality control may represent competing tasks.