Calcium Signalling and Mitochondrial Motility

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. György Hajnóczky,
  2. Masao Saotome,
  3. György Csordás,
  4. David Weaver and
  5. Muqing Yi

Published Online: 20 MAY 2008

DOI: 10.1002/9780470725207.ch8

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

How to Cite

Hajnóczky, G., Saotome, M., Csordás, G., Weaver, D. and Yi, M. (2007) Calcium Signalling and Mitochondrial Motility, in Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470725207.ch8

Author Information

  1. Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Rm 253 7AH, 1020 Locust Street, Philadelphia, PA 19107, USA

Publication History

  1. Published Online: 20 MAY 2008
  2. Published Print: 5 OCT 2007

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470066577

Online ISBN: 9780470725207

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Keywords:

  • mitochondria;
  • ER;
  • Ca2+;
  • calcium signalling;
  • motility;
  • microtubule;
  • microfilament

Summary

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 Ca2+-dependent cell survival and cell death mechanisms.