|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
First published online 13 February 2007
doi: 10.1242/jcs.03381
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Research Article |
1 Institut National de la Santé et de la Recherche Médicale (INSERM), U688 Physiopathologie Mitochondriale, Universite Victor Segalen-Bordeaux 2, 146 rue Leo-Saignat, F-33076 Bordeaux cedex, France
2 Department of Cell Biology, University of Geneva, 30, Quai Ansermet 1211 Geneva 4, Switzerland
3 Laboratoire de Biologie Moleculaire et de Sequencage, Institut de Biochimie et Genetique Cellulaires, UMR Universite Victor Segalen Bordeaux 2-CNRS 5095, box 64, 146 rue Leo Saignat, F-33076 Bordeaux Cedex, France
* Author for correspondence (e-mail: rossig{at}u-bordeaux2.fr)
Accepted 13 December 2006
Mitochondria form a dynamic network, and it remains unclear how the alternate configurations interact with bioenergetics properties. The metabolic signals that link mitochondrial structure to its functional states have not been fully characterized. In this report, we analyze the bidirectional relationships between mitochondrial morphology and function in living human cells. First, we determined the effect of mitochondrial fission on energy production by using small interfering RNA (siRNA) targeting DRP1, which revealed the importance of membrane fluidity on the control of bioenergetics. Second, we followed the effect of rotenone, a specific inhibitor of respiratory chain complex I, which causes large structural perturbations, once a threshold was reached. Last, we followed changes in the mitochondrial network configuration in human cells that had been treated with modulators of oxidative phosphorylation, and in fibroblasts from two patients with mitochondrial disease where the respiratory rate, 
and the generation of reactive oxygen species (ROS) were measured. Our data demonstrate that the relationship between mitochondrial network organization and bioenergetics is bidirectional, and we provide a model for analyzing the metabolic signals involved in this crosstalk.
Key words: Mitochondrial network, Fission, DRP1, Oxidative phosphorylation, Threshold effect
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati
Twitter What's this?
Related articles in JCS:
This article has been cited by other articles:
![]() |
X. Wang, B. Su, H.-g. Lee, X. Li, G. Perry, M. A. Smith, and X. Zhu Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's Disease J. Neurosci., July 15, 2009; 29(28): 9090 - 9103. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Liesa, M. Palacin, and A. Zorzano Mitochondrial Dynamics in Mammalian Health and Disease Physiol Rev, July 1, 2009; 89(3): 799 - 845. [Abstract] [Full Text] [PDF] |
||||
![]() |
K.-S. Park, A. Wiederkehr, C. Kirkpatrick, Y. Mattenberger, J.-C. Martinou, P. Marchetti, N. Demaurex, and C. B. Wollheim Selective Actions of Mitochondrial Fission/Fusion Genes on Metabolism-Secretion Coupling in Insulin-releasing Cells J. Biol. Chem., November 28, 2008; 283(48): 33347 - 33356. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. J. H. Koopman, F. Distelmaier, M. A. Hink, S. Verkaart, M. Wijers, J. Fransen, J. A. M. Smeitink, and P. H. G. M. Willems Inherited complex I deficiency is associated with faster protein diffusion in the matrix of moving mitochondria Am J Physiol Cell Physiol, May 1, 2008; 294(5): C1124 - C1132. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. C. Poole, R. E. Thomas, L. A. Andrews, H. M. McBride, A. J. Whitworth, and L. J. Pallanck The PINK1/Parkin pathway regulates mitochondrial morphology PNAS, February 5, 2008; 105(5): 1638 - 1643. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. Parra, V. Eisner, M. Chiong, A. Criollo, F. Moraga, A. Garcia, S. Hartel, E. Jaimovich, A. Zorzano, C. Hidalgo, et al. Changes in mitochondrial dynamics during ceramide-induced cardiomyocyte early apoptosis Cardiovasc Res, January 15, 2008; 77(2): 387 - 397. [Abstract] [Full Text] [PDF] |
||||