OPA1 alternate splicing uncouples an evolutionary conserved function in mitochondrial fusion from a vertebrate restricted function in apoptosis.
Cell Death Differ
; 14(4): 682-92, 2007 Apr.
Article
em En
| MEDLINE
| ID: mdl-17024226
ABSTRACT
In most eucaryote cells, release of apoptotic proteins from mitochondria involves fission of the mitochondrial network and drastic remodelling of the cristae structures. The intramitochondrial dynamin OPA1, as a potential central actor of these processes, exists as eight isoforms resulting from the alternate splicing combinations of exons (Ex) 4, 4b and 5b, which functions remain undetermined. Here, we show that Ex4 that is conserved throughout evolution confers functions to OPA1 involved in the maintenance of the DeltaPsi(m) and in the fusion of the mitochondrial network. Conversely, Ex4b and Ex5b, which are vertebrate specific, define a function involved in cytochrome c release, an apoptotic process also restricted to vertebrates. The drastic changes of OPA1 variant abundance in different organs suggest that nuclear splicing can control mitochondrial dynamic fate and susceptibility to apoptosis and pathologies.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Leveduras
/
Células HeLa
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Apoptose
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Processamento Alternativo
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Proteínas Mitocondriais
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GTP Fosfo-Hidrolases
Limite:
Animals
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Humans
Idioma:
En
Revista:
Cell Death Differ
Ano de publicação:
2007
Tipo de documento:
Article