title: Mechanics of mitochondrial motility in neurons.
abstract: A properly organized, healthy mitochondrial network is critical for preserving neuronal form and function. Large, elaborately branched neuronal morphologies, energetic demands that fluctuate in time and space, and long neuronal lifespans make the distribution of mitochondria in neurons a particularly complex problem. Moreover, mitochondrial networks are dynamic systems in which mitochondria grow, divide and fuse, move along cytoskeletal filaments, and are degraded in an active fashion. Although the molecular mechanisms that govern mitochondrial motility, in particular, are increasingly well-characterized, the manner in which these mechanisms are coordinated to give rise to the global mitochondrial distribution in neurons is less well understood. Here I review several molecular mechanisms for mitochondrial motility in the context of a general mechanical framework. In this framework, molecular pathways that control mitochondrial movement can be reduced to their effects on the balance of forces that act on mitochondria, driving and opposing movement.
authors.affiliation: Department of Neurobiology, Stanford University School of Medicine, Laboratory of Thomas Clandinin, Fairchild Building, D217, 299 Campus Drive West, Stanford, CA 94305, USA. Electronic address: ebarnhar@stanford.edu.
authors.forename: Erin L
authors.initials: EL
authors.lastname: Barnhart
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism; D001692:Biological Transport; D001696:Biomechanical Phenomena; D003599:Cytoskeleton / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*