Cardiolipin remodeling enables protein crowding in the inner mitochondrial membrane.
Acyltransferases
/ physiology
Animals
Cardiolipins
/ chemistry
Drosophila melanogaster
Fatty Acids
/ metabolism
Female
Liposomes
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondria, Heart
/ metabolism
Mitochondria, Muscle
/ metabolism
Mitochondrial Membranes
/ metabolism
Oxidation-Reduction
Oxidative Phosphorylation
Proteins
/ metabolism
Saccharomyces cerevisiae
Barth syndrome
lipid-protein interaction
macromolecular crowding
mitochondria
oxidative phosphorylation
Journal
The EMBO journal
ISSN: 1460-2075
Titre abrégé: EMBO J
Pays: England
ID NLM: 8208664
Informations de publication
Date de publication:
01 12 2021
01 12 2021
Historique:
revised:
23
09
2021
received:
07
04
2021
accepted:
24
09
2021
pubmed:
19
10
2021
medline:
22
12
2021
entrez:
18
10
2021
Statut:
ppublish
Résumé
Mitochondrial cristae are extraordinarily crowded with proteins, which puts stress on the bilayer organization of lipids. We tested the hypothesis that the high concentration of proteins drives the tafazzin-catalyzed remodeling of fatty acids in cardiolipin, thereby reducing bilayer stress in the membrane. Specifically, we tested whether protein crowding induces cardiolipin remodeling and whether the lack of cardiolipin remodeling prevents the membrane from accumulating proteins. In vitro, the incorporation of large amounts of proteins into liposomes altered the outcome of the remodeling reaction. In yeast, the concentration of proteins involved in oxidative phosphorylation (OXPHOS) correlated with the cardiolipin composition. Genetic ablation of either remodeling or biosynthesis of cardiolipin caused a substantial drop in the surface density of OXPHOS proteins in the inner membrane of the mouse heart and Drosophila flight muscle mitochondria. Our data suggest that OXPHOS protein crowding induces cardiolipin remodelling and that remodeled cardiolipin supports the high concentration of these proteins in the inner mitochondrial membrane.
Identifiants
pubmed: 34661298
doi: 10.15252/embj.2021108428
pmc: PMC8634138
doi:
Substances chimiques
Cardiolipins
0
Fatty Acids
0
Liposomes
0
Proteins
0
Acyltransferases
EC 2.3.-
tafazzin protein, mouse
EC 2.3.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e108428Subventions
Organisme : NCI NIH HHS
ID : P30 CA016087
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM115593
Pays : United States
Organisme : NINDS NIH HHS
ID : P30 NS050276
Pays : United States
Organisme : NIH HHS
ID : S10 OD023659
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR027990
Pays : United States
Informations de copyright
© 2021 The Authors.
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