Abstract:
:Cytochrome c release from mitochondria promotes apoptosome formation and caspase activation. The question as to whether mitochondrial permeabilization kills cells via a caspase-independent pathway when caspase activation is prevented is still open. Here we report that proneural cells of embryonic origin, when induced to die but rescued by apoptosome inactivation are deprived of cytosolic cytochrome c through proteasomal degradation. We also show that, in this context, those cells keep generating ATP by glycolysis for a long period of time and that they keep their mitochondria in a depolarized state that can be reverted. Moreover, under these conditions, such apoptosome-deficient cells activate a Beclin 1-dependent autophagy pathway to sustain glycolytic-dependent ATP production. Our findings contribute to elucidating what the point-of-no-return in apoptosis is. They also help in clarifying the issue of survival of apoptosome-deficient proneural cells under stress conditions. Unraveling this issue could be highly relevant for pharmacological intervention and for therapies based on neural stem cell transfer in the treatment of neurological disorders.
journal_name
Mol Biol Celljournal_title
Molecular biology of the cellauthors
Ferraro E,Pulicati A,Cencioni MT,Cozzolino M,Navoni F,di Martino S,Nardacci R,Carrì MT,Cecconi Fdoi
10.1091/mbc.e07-09-0858subject
Has Abstractpub_date
2008-08-01 00:00:00pages
3576-88issue
8eissn
1059-1524issn
1939-4586pii
E07-09-0858journal_volume
19pub_type
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