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J. Cell Biol.,
Volume 144, Number 4, February 22, 1999 701-710
* Department of Cell Biology and Neuroscience, University of Texas, Southwestern Medical Center, Dallas, Texas 75235-9039;
and Drosophila affords a genetically well-defined
system to study apoptosis in vivo. It offers a powerful
extension to in vitro models that have implicated a requirement for cytochrome c in caspase activation and
apoptosis. We found that an overt alteration in cytochrome c anticipates programmed cell death (PCD) in
Drosophila tissues, occurring at a time that considerably precedes other known indicators of apoptosis. The
altered configuration is manifested by display of an otherwise hidden epitope and occurs without release of the
protein into the cytosol. Conditional expression of the Drosophila death activators, reaper or grim, provoked
apoptogenic cytochrome c display and, surprisingly,
caspase activity was necessary and sufficient to induce
this alteration. In cell-free studies, cytosolic caspase activation was triggered by mitochondria from apoptotic
cells but identical preparations from healthy cells were
inactive. Our observations provide compelling validation of an early role for altered cytochrome c in PCD
and suggest propagation of apoptotic physiology
through reciprocal, feed-forward amplification involving cytochrome c and caspases.
Department of Microbiology and Center for Immunology, University of Minnesota Medical School, Minneapolis,
Minnesota 55455
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