Apoptosis in Drosophila: neither fish nor fowl (nor man, nor worm).
Abstract
Studies in a wide variety of organisms have produced a general model for the induction
of apoptosis in which multiple signaling pathways lead ultimately to activation of
the caspase family of proteases. Once activated, these enzymes cleave key cellular
substrates to promote the orderly dismantling of dying cells. A broad similarity exists
in the cell death pathways operating in different organisms and there is a clear evolutionary
conservation of apoptotic regulators such as caspases, Bcl-2 family members, inhibitor
of apoptosis (IAP) proteins, IAP antagonists and caspase activators. Despite this,
studies in Caenorhabditis elegans, Drosophila and vertebrates have revealed some apparent
differences both in the way apoptosis is regulated and in the way individual molecules
contribute to the propagation of the death signal. For example, whereas cytochrome
c released from mitochondria clearly promotes caspase activation in vertebrates, there
is no documented role for cytochrome c in C. elegans apoptosis and its role in Drosophila
is highly controversial. In addition, the apoptotic potency of IAP antagonists appears
to be greater in Drosophila than in vertebrates, indicating that IAPs may be of different
relative importance in different organisms. Thus, although Drosophila, worms and humans
share a host of apoptotic regulators, the way in which they function may not be identical.
Type
Journal articleSubject
AnimalsApoptosis
Caspases
Cytochromes c
Drosophila melanogaster
Enzyme Inhibitors
Humans
Models, Biological
Proto-Oncogene Proteins c-bcl-2
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https://hdl.handle.net/10161/8399Published Version (Please cite this version)
10.1242/jcs.02377Publication Info
Kornbluth, Sally; & White, Kristin (2005). Apoptosis in Drosophila: neither fish nor fowl (nor man, nor worm). J Cell Sci, 118(Pt 9). pp. 1779-1787. 10.1242/jcs.02377. Retrieved from https://hdl.handle.net/10161/8399.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Sally A. Kornbluth
Jo Rae Wright University Distinguished Professor
Our lab studies the regulation of complex cellular processes, including cell cycle
progression and programmed cell death (apoptosis). These tightly orchestrated processes
are critical for appropriate cell proliferation and cell death, and when they go awry
can result in cancer and degenerative disorders. Within these larger fields, we have
focused on understanding the cellular mechanisms that prevent the onset of mitosis
prior to the completion of DNA replication, the process

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