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In vivo mutagenesis reveals that OriL is essential for mitochondrial DNA replication.
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- Wanrooij, Sjoerd (author)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
- Miralles Fusté, Javier (author)
- Stewart, James B (author)
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- Wanrooij, Paulina H (author)
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- (creator_code:org_t)
- 2012-10-23
- 2012
- English.
- In: EMBO reports. - : EMBO. - 1469-3178 .- 1469-221X. ; 13:12, s. 1130-7
- Journal article (peer-reviewed)
Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
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