Talk:Cell Mitochondria

From CellBiology
Revision as of 21:20, 28 March 2011 by S8600021 (talk | contribs) (Created page with " ===Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process=== J Cell Bio...")
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)

Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process

J Cell Biol. 2001 Apr 16;153(2):319-28.

Waterhouse NJ, Goldstein JC, von Ahsen O, Schuler M, Newmeyer DD, Green DR.

Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, California 92121, USA.

Abstract

During apoptosis, cytochrome c is released into the cytosol as the outer membrane of mitochondria becomes permeable, and this acts to trigger caspase activation. The consequences of this release for mitochondrial metabolism are unclear. Using single-cell analysis, we found that when caspase activity is inhibited, mitochondrial outer membrane permeabilization causes a rapid depolarization of mitochondrial transmembrane potential, which recovers to original levels over the next 30-60 min and is then maintained. After outer membrane permeabilization, mitochondria can use cytoplasmic cytochrome c to maintain mitochondrial transmembrane potential and ATP production. Furthermore, both cytochrome c release and apoptosis proceed normally in cells in which mitochondria have been uncoupled. These studies demonstrate that cytochrome c release does not affect the integrity of the mitochondrial inner membrane and that, in the absence of caspase activation, mitochondrial functions can be maintained after the release of cytochrome c.

PMID: 11309413 http://www.ncbi.nlm.nih.gov/pubmed/11309413

J. Cell Biol. Vol. 153 No. 2 p.319

Waterhouse et al.

Video 1 (1.5MB)

Loss and regeneration of {Delta}{Psi}m after cytochrome c release. Cc-GFP-HeLa cells were treated with actinomycin D (1 µM) in the presence of N-benzoylcarbonyl-Val-Ala-Asp-fluorome-thylketone (zVADfmk) (100 µM), and confocal images were taken every 2 min. The cytochrome c-GFP (green, left) shows the coordinate release of cytochrome c in the individual cells (the staining goes from punctate to diffuse upon release). TMRE fluorescence in the same cells (red, right) shows the loss and recovery of {Delta}{Psi}m. The red and green images are of the same cells taken at the same time. The frames are separate rather than overlaid for clarity, and a mathematical representation of loss and regen-eration of {Delta}{Psi}m in a similarly treated cell is shown in Fig. 4 A.