Journal
JOURNAL OF CELL BIOLOGY
Volume 153, Issue 2, Pages 319-328Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.153.2.319
Keywords
apoptosis; mitochondria; membrane potential; caspases; ATP
Categories
Funding
- NCI NIH HHS [CA69381] Funding Source: Medline
- NIAID NIH HHS [AI40646] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available