![]() ![]() Opa1 mediates mitochondrial inner membrane fusion. Mitofusins mediate mitochondrial outer membrane fusion in mammals. Mitochondrial fission and fusion are now considered cornerstones for cell survival because of their contributions to health and disease.įunctions of the mitochondrial Dynamin family members. However, in more recent years, the biological relevance of these phenomena has become clear with the discovery of human diseases that are caused by mutations in fission and fusion proteins and the discovery of numerous connections with apoptosis and mitophagy ( Westermann 2010 Chan 2012 Nunnari and Suomalainen 2012 Youle and van der Bliek 2012). Obvious reasons, such as accommodating cell growth, cell division, and the redistribution of mitochondria during differentiation, did not fully explain why mitochondria fuse nor did they explain the high frequencies of these occurrences. The importance of frequent mitochondrial fission and fusion events for cell survival was also not fully appreciated until fairly recently. Because of these morphological changes mitochondria are now known to be very dynamic. In some cells they fuse together, forming a single closed network, whereas in other cells or under different circumstances mitochondria convert into large numbers of small fragments. Mitochondrial morphologies can change dramatically by shifting this balance. Their lengths are determined by the balance between fission and fusion. 1981 Bereiter-Hahn and Voth 1994 Rizzuto et al. Careful observations, first with phase contrast microscopy, then with vital dyes and finally with targeted fluorescent proteins, showed that mitochondria continually divide and fuse, even in resting cells ( Johnson et al. Renewed appreciation for mitochondrial dynamics emerged some 20 or 30 years ago when technological advances made it much easier to track mitochondria in live cells. For a long time, these observations remained something of a curiosity and they were all but forgotten when electron microscopy popularized the idea that mitochondria exist as isolated sausage-shaped organelles floating in a sea of cytoplasm. All rights reserved.Mitochondrial movement and fission were first observed with light microscopy almost 100 years ago ( Lewis and Lewis 1914). We suggest that deeper understanding of the regulatory mechanisms within this system and downstream implications could benefit in understanding and intervention of these conditions.Īge-related disease Aging Fission Fusion Mitochondrial dynamics.Ĭopyright © 2020 The Author(s). Finally, we discuss the current evidence implicating these processes in age-related human pathologies, such as neurodegenerative or cardio-metabolic diseases. Here, we discuss the mechanisms of mitochondrial fission and fusion, the current evidence of their role in aging of multicellular organisms, and how these connect to cell cycle regulation, quality control, and transmission of energy status. There does exist, however, a large body of evidence connecting mitochondrial dynamics to other aging-related cellular processes and implicates them in a number of human diseases. While many mitochondrial processes are already characterized in relation to aging, specific evidence in multicellular organisms causally linking mitochondrial dynamics to the regulation of lifespan is limited. Mitochondria separate and merge using fission and fusion processes in response to changes in energy and stress status. Crucial to mitochondrial regulation is the dynamic nature of their network structure. Dysregulation of mitochondrial function is one of the classical hallmarks of aging, and mitochondrial interventions have repeatedly been shown to improve outcomes in age-related diseases. The mitochondria is the major hub to convert energy for cellular processes. ![]()
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