OPA1 alternate splicing uncouples an evolutionary conserved function in mitochondrial fusion from a vertebrate restricted function in apoptosis. - CNRS - Centre national de la recherche scientifique Accéder directement au contenu
Article Dans Une Revue Cell Death and Differentiation Année : 2007

OPA1 alternate splicing uncouples an evolutionary conserved function in mitochondrial fusion from a vertebrate restricted function in apoptosis.

Résumé

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.
Fichier principal
Vignette du fichier
Olichon_OPA1_alternate.pdf (5.65 Mo) Télécharger le fichier
Loading...

Dates et versions

inserm-00164127 , version 1 (06-03-2008)

Identifiants

Citer

Aurélien Olichon, Ghizlane Elachouri, Laurent Baricault, Cécile Delettre, Pascale Belenguer, et al.. OPA1 alternate splicing uncouples an evolutionary conserved function in mitochondrial fusion from a vertebrate restricted function in apoptosis.: OPA1 isoforms in mitochondrial fusion or apoptosis.. Cell Death and Differentiation, 2007, 14 (4), pp.682-92. ⟨10.1038/sj.cdd.4402048⟩. ⟨inserm-00164127⟩
98 Consultations
229 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More