Ablation of mitochondrial DNA results in widespread remodeling of the mitochondrial complexome
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Ablation of mitochondrial DNA results in widespread remodeling of the mitochondrial complexome. / Guerrero-Castillo, Sergio; van Strien, Joeri; Brandt, Ulrich; Arnold, Susanne.
In: EMBO J, Vol. 40, No. 21, 02.11.2021, p. e108648.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Ablation of mitochondrial DNA results in widespread remodeling of the mitochondrial complexome
AU - Guerrero-Castillo, Sergio
AU - van Strien, Joeri
AU - Brandt, Ulrich
AU - Arnold, Susanne
N1 - © 2021 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
PY - 2021/11/2
Y1 - 2021/11/2
N2 - So-called ρ0 cells lack mitochondrial DNA and are therefore incapable of aerobic ATP synthesis. How cells adapt to survive ablation of oxidative phosphorylation remains poorly understood. Complexome profiling analysis of ρ0 cells covered 1,002 mitochondrial proteins and revealed changes in abundance and organization of numerous multiprotein complexes including previously not described assemblies. Beyond multiple subassemblies of complexes that would normally contain components encoded by mitochondrial DNA, we observed widespread reorganization of the complexome. This included distinct changes in the expression pattern of adenine nucleotide carrier isoforms, other mitochondrial transporters, and components of the protein import machinery. Remarkably, ablation of mitochondrial DNA hardly affected the complexes organizing cristae junctions indicating that the altered cristae morphology in ρ0 mitochondria predominantly resulted from the loss of complex V dimers required to impose narrow curvatures to the inner membrane. Our data provide a comprehensive resource for in-depth analysis of remodeling of the mitochondrial complexome in response to respiratory deficiency.
AB - So-called ρ0 cells lack mitochondrial DNA and are therefore incapable of aerobic ATP synthesis. How cells adapt to survive ablation of oxidative phosphorylation remains poorly understood. Complexome profiling analysis of ρ0 cells covered 1,002 mitochondrial proteins and revealed changes in abundance and organization of numerous multiprotein complexes including previously not described assemblies. Beyond multiple subassemblies of complexes that would normally contain components encoded by mitochondrial DNA, we observed widespread reorganization of the complexome. This included distinct changes in the expression pattern of adenine nucleotide carrier isoforms, other mitochondrial transporters, and components of the protein import machinery. Remarkably, ablation of mitochondrial DNA hardly affected the complexes organizing cristae junctions indicating that the altered cristae morphology in ρ0 mitochondria predominantly resulted from the loss of complex V dimers required to impose narrow curvatures to the inner membrane. Our data provide a comprehensive resource for in-depth analysis of remodeling of the mitochondrial complexome in response to respiratory deficiency.
KW - Adaptation, Physiological
KW - Adenosine Triphosphate/metabolism
KW - Cell Line, Tumor
KW - DNA, Mitochondrial/genetics
KW - Gene Expression
KW - Humans
KW - Mitochondria/metabolism
KW - Mitochondrial Membranes/chemistry
KW - Mitochondrial Proteins/deficiency
KW - Multiprotein Complexes/deficiency
KW - Osteoblasts/metabolism
KW - Oxidative Phosphorylation
U2 - 10.15252/embj.2021108648
DO - 10.15252/embj.2021108648
M3 - SCORING: Journal article
C2 - 34542926
VL - 40
SP - e108648
JO - EMBO J
JF - EMBO J
SN - 0261-4189
IS - 21
ER -