Mitochondrial Fusion and Fission in Health and Disease
David C. Chan Division of Biology and Biological Engineering, California Institute of Technology Pasadena, CA, USA
Mitochondria are essential organelles that undergo continual cycles of fusion, fission, and regulated degradation. These dynamic processes play critical roles in maintaining the quality of the mitochondrial population in cells. Human genetic studies have shown that mutations in mitochondrial fusion or fission genes can affect multiple tissues and cause disease. Mutations in Mfn2, a molecule involved in mitochondrial outer membrane fusion, cause Charcot-Marie-Tooth type 2A, and mutations in Opa1, a molecule involved in mitochondrial inner membrane fusion, cause dominant optic atrophy. Moreover, mutations in Drp1, essential for mitochondrial fission, can cause a variety of clinical disorders, ranging from early neonatal lethality to intractable epilepsy in early childhood. I will discuss how defects in mitochondrial dynamics impact human health, with insights from mouse and cellular studies. In addition, I will discuss our attempts to identify new quality control pathways in mitochondria.
Credits: None available.
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