TY  - JOUR
A1  - Weber, Tobias Alexander
A1  - Koob, Sebastian
A1  - Heide, Heinrich
A1  - Wittig, Ilka
A1  - Head, Brian
A1  - Bliek, Alexander van der
A1  - Brandt, Ulrich
A1  - Mittelbronn, Michel Guy André
A1  - Reichert, Andreas
T1  - APOOL is a cardiolipin-binding component of the Mitofilin/MINOS protein complex determining cristae morphology in mammalian mitochondria
T2  - PLoS One
N2  - Mitochondrial cristae morphology is highly variable and altered under numerous pathological conditions. The protein complexes involved are largely unknown or only insufficiently characterized. Using complexome profiling we identified apolipoprotein O (APOO) and apolipoprotein O-like protein (APOOL) as putative components of the Mitofilin/MINOS protein complex which was recently implicated in determining cristae morphology. We show that APOOL is a mitochondrial membrane protein facing the intermembrane space. It specifically binds to cardiolipin in vitro but not to the precursor lipid phosphatidylglycerol. Overexpression of APOOL led to fragmentation of mitochondria, a reduced basal oxygen consumption rate, and altered cristae morphology. Downregulation of APOOL impaired mitochondrial respiration and caused major alterations in cristae morphology. We further show that APOOL physically interacts with several subunits of the MINOS complex, namely Mitofilin, MINOS1, and SAMM50. We conclude that APOOL is a cardiolipin-binding component of the Mitofilin/MINOS protein complex determining cristae morphology in mammalian mitochondria. Our findings further assign an intracellular role to a member of the apolipoprotein family in mammals.
Y1  - 2013
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30051
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-300513
SN  - 1932-6203
N1  - Copyright: © 2013 Weber et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
VL  - 8
IS  - (5):e63683
PB  - PLoS
CY  - Lawrence, Kan.
ER  -