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Mitochondrial Rhomboid PARL Regulates Cytochrome c Release during Apoptosis via OPA1-Dependent Cristae Remodeling

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Cipolat, Sara, Rudka, Tomasz, Hartmann, Dieter, Costa, Veronica, Serneels, Lutgarde, Craessaerts, Katleen, Metzger, Kristine, Frezza, Christian, Annaert, Wim, D'Adamio, Luciano, Derks, Carmen, Dejaegere, Tim, Pellegrini, Luca, D'Hooge, Rudi, Scorrano, Luca, De Strooper, Bart·2006·Cell
DOI 10.1016/j.cell.2006.06.021
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Abstract

Rhomboids, evolutionarily conserved integral membrane proteases, participate in crucial signaling pathways. Presenilin-associated rhomboid-like (PARL) is an inner mitochondrial membrane rhomboid of unknown function, whose yeast ortholog is involved in mitochondrial fusion. Parl-/- mice display normal intrauterine development but from the fourth postnatal week undergo progressive multisystemic atrophy leading to cachectic death. Atrophy is sustained by increased apoptosis, both in and ex vivo. Parl-/- cells display normal mitochondrial morphology and function but are no longer protected against intrinsic apoptotic death stimuli by the dynamin-related mitochondrial protein OPA1. Parl-/- mitochondria display reduced levels of a soluble, intermembrane space (IMS) form of OPA1, and OPA1 specifically targeted to IMS complements Parl-/- cells, substantiating the importance of PARL in OPA1 processing. Parl-/- mitochondria undergo faster apoptotic cristae remodeling and cytochrome c release. These findings implicate regulated intramembrane proteolysis in controlling apoptosis.

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Cited by

Metadata

Authors
Cipolat, S., Rudka, T., Hartmann, D., Costa, V., Serneels, L., Craessaerts, K., Metzger, K., Frezza, C., Annaert, W., D'Adamio, L., Derks, C., Dejaegere, T., Pellegrini, L., D'Hooge, R., Scorrano, L., & De Strooper, B.
Venue
Cell
Publisher
Elsevier BV
Published
2006-07
Volume
126
Issue
1
Pages
163-175
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/j.cell.2006.06.021
OpenAlex
W1979489548
Cited by
741
References
4
FWCI
22.47
Type
journal article
Language
en
Open access
bronze
Licence

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