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  Mitochondrial fusion is required for regulation of mitochondrial DNA replication.

Ramos, E. S., Motori, E., Brüser, C., Kühl, I., Yeroslaviz, A., Ruzzenente, B., et al. (2019). Mitochondrial fusion is required for regulation of mitochondrial DNA replication. PLoS Genetics, 15(6): e1008085. doi:10.1371/journal.pgen.1008085.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0003-CB3D-5 Version Permalink: http://hdl.handle.net/21.11116/0000-0003-CB44-C
Genre: Journal Article

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 Creators:
Ramos, E. S., Author
Motori, E., Author
Brüser, C.1, Author              
Kühl, I., Author
Yeroslaviz, A., Author
Ruzzenente, B., Author
Kauppila, J. H. K., Author
Busch, J. D., Author
Hultenby, K., Author
Habermann, B. H., Author
Jakobs, S.1, Author              
Larsson, N. G., Author
Mourier, A., Author
Affiliations:
1Research Group of Mitochondrial Structure and Dynamics, MPI for Biophysical Chemistry, Max Planck Society, ou_578566              

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 Abstract: Mitochondrial dynamics is an essential physiological process controlling mitochondrial content mixing and mobility to ensure proper function and localization of mitochondria at intracellular sites of high-energy demand. Intriguingly, for yet unknown reasons, severe impairment of mitochondrial fusion drastically affects mtDNA copy number. To decipher the link between mitochondrial dynamics and mtDNA maintenance, we studied mouse embryonic fibroblasts (MEFs) and mouse cardiomyocytes with disruption of mitochondrial fusion. Super-resolution microscopy revealed that loss of outer mitochondrial membrane (OMM) fusion, but not inner mitochondrial membrane (IMM) fusion, leads to nucleoid clustering. Remarkably, fluorescence in situ hybridization (FISH), bromouridine labeling in MEFs and assessment of mitochondrial transcription in tissue homogenates revealed that abolished OMM fusion does not affect transcription. Furthermore, the profound mtDNA depletion in mouse hearts lacking OMM fusion is not caused by defective integrity or increased mutagenesis of mtDNA, but instead we show that mitochondrial fusion is necessary to maintain the stoichiometry of the protein components of the mtDNA replisome. OMM fusion is necessary for proliferating MEFs to recover from mtDNA depletion and for the marked increase of mtDNA copy number during postnatal heart development. Our findings thus link OMM fusion to replication and distribution of mtDNA.

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Language(s): eng - English
 Dates: 2019-06-06
 Publication Status: Published online
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 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1371/journal.pgen.1008085
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Title: PLoS Genetics
Source Genre: Journal
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Pages: 28 Volume / Issue: 15 (6) Sequence Number: e1008085 Start / End Page: - Identifier: -