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

Journal article
Authors Sjoerd Wanrooij
Javier Miralles Fusté
James B Stewart
Paulina H Wanrooij
Tore Samuelsson
Nils-Göran Larsson
Claes M Gustafsson
Maria Falkenberg
Published in EMBO reports
Volume 13
Issue 12
Pages 1130-7
ISSN 1469-3178
Publication year 2012
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 1130-7
Language en
Links dx.doi.org/10.1038/embor.2012.161
Subject categories Cell and Molecular Biology, Medical cell biology

Abstract

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.

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