title: Calcium signalling and mitochondrial motility.
abstract: Intracellular Ca2+ is able to control numerous cellular responses through complex spatial and temporal organization. For the effective handling of intracellular Ca2+, endoplasmic reticulum (ER) Ca2+ mobilization and plasma membrane Ca2+ entry have to be complemented by strategic and dynamic positioning of an energy source that is usually provided by mitochondrial ATP production. Mitochondria also participate in the transport of Ca2+. Mitochondria are dynamically distributed in cells and utilize cytoskeletal tracks and motor proteins for their movements. Recent studies have reported that Ca2+ inhibits mitochondrial motility providing a mechanism to retain mitochondria at Ca2+ signalling sites. Here we discuss the control of the mitochondrial distribution by cell signalling mechanisms, the spatial relationship among individual mitochondria and ER domains, and the possible implications of mitochondrial movements in the Ca(2+)-dependent cell survival and cell death mechanisms.
authors: Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
authors: György
authors: G
authors: Hajnóczky
authors: Masao
authors: M
authors: Saotome
authors: György
authors: G
authors: Csordás
authors: David
authors: D
authors: Weaver
authors: Muqing
authors: M
authors: Yi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000502:physiology*
chemical_list: D002118:Calcium