In vivo mutagenesis reveals that OriL is essential for mitochondrial DNA 
replication

Wanrooij, S.; Miralles Fuste, J.; Stewart, J.; Wanrooij, P. H.; Samuelsson, T.; Larsson, N. G.; Gustafsson, C. M.; Falkenberg, M.

doi:10.1038/embor.2012.161

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In vivo mutagenesis reveals that OriL is essential for mitochondrial DNA replication

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Stewart, J.
Stewart – Mitochondrial Mutations and Genome Co-evolution, Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

Externe Ressourcen

https://www.ncbi.nlm.nih.gov/pubmed/23090476
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Zitation

Wanrooij, S., Miralles Fuste, J., Stewart, J., Wanrooij, P. H., Samuelsson, T., Larsson, N. G., et al. (2012). In vivo mutagenesis reveals that OriL is essential for mitochondrial DNA replication. EMBO Rep, 13(12), 1130-7. doi:10.1038/embor.2012.161.

Zitierlink: https://hdl.handle.net/21.11116/0000-000B-6943-4

Zusammenfassung

The mechanisms of mitochondrial DNA replication have been hotly debated for a decade. The strand-displacement model states that lagging-strand DNA synthesis is initiated from the origin of light-strand DNA replication (OriL), whereas the strand-coupled model implies that OriL is dispensable. Mammalian mitochondria cannot be transfected and the requirements of OriL in vivo have therefore not been addressed. We here use in vivo saturation mutagenesis to demonstrate that OriL is essential for mtDNA maintenance in the mouse. Biochemical and bioinformatic analyses show that OriL is functionally conserved in vertebrates. Our findings strongly support the strand-displacement model for mtDNA replication.