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本文引用的文献

1
Mitochondrial transfection for studying organellar DNA repair, genome maintenance and aging.线粒体转染在研究细胞器 DNA 修复、基因组维护和衰老中的应用。
Mech Ageing Dev. 2011 Aug;132(8-9):412-23. doi: 10.1016/j.mad.2011.05.002. Epub 2011 May 27.
2
Mitochondrial DNA replication and disease: insights from DNA polymerase γ mutations.线粒体 DNA 复制与疾病：DNA 聚合酶 γ 突变的启示。
Cell Mol Life Sci. 2011 Jan;68(2):219-33. doi: 10.1007/s00018-010-0530-4. Epub 2010 Oct 8.
3
The human mitochondrial replication fork in health and disease.健康与疾病中的人类线粒体复制叉
Biochim Biophys Acta. 2010 Aug;1797(8):1378-88. doi: 10.1016/j.bbabio.2010.04.015. Epub 2010 Apr 22.
4
Mitochondrial RNA polymerase is needed for activation of the origin of light-strand DNA replication.线粒体 RNA 聚合酶是轻链 DNA 复制起始激活所必需的。
Mol Cell. 2010 Jan 15;37(1):67-78. doi: 10.1016/j.molcel.2009.12.021.
5
Infernal 1.0: inference of RNA alignments.Infernal 1.0：RNA比对推断
Bioinformatics. 2009 May 15;25(10):1335-7. doi: 10.1093/bioinformatics/btp157. Epub 2009 Mar 23.
6
UNAFold: software for nucleic acid folding and hybridization.UNAFold：用于核酸折叠和杂交的软件。
Methods Mol Biol. 2008;453:3-31. doi: 10.1007/978-1-60327-429-6_1.
7
Human mitochondrial RNA polymerase primes lagging-strand DNA synthesis in vitro.人线粒体RNA聚合酶在体外引发滞后链DNA合成。
Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11122-7. doi: 10.1073/pnas.0805399105. Epub 2008 Aug 6.
8
Replication of mitochondrial DNA occurs by strand displacement with alternative light-strand origins, not via a strand-coupled mechanism.线粒体DNA的复制通过链置换和交替轻链起始点进行，而非通过链偶联机制。
Genes Dev. 2005 Oct 15;19(20):2466-76. doi: 10.1101/gad.1352105.
9
A bidirectional origin of replication maps to the major noncoding region of human mitochondrial DNA.一个双向复制起点定位于人类线粒体DNA的主要非编码区域。
Mol Cell. 2005 Jun 10;18(6):651-62. doi: 10.1016/j.molcel.2005.05.002.
10
The mitochondrial RNA polymerase contributes critically to promoter specificity in mammalian cells.线粒体RNA聚合酶对哺乳动物细胞中的启动子特异性起着关键作用。
EMBO J. 2004 Nov 24;23(23):4606-14. doi: 10.1038/sj.emboj.7600465. Epub 2004 Nov 4.

体内诱变揭示 OriL 对于线粒体 DNA 复制是必需的。

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

机构信息

Department of Medical Biochemistry and Cell Biology, University of Gothenburg, P.O. Box 440, SE-405 30 Gothenburg, Sweden.

出版信息

EMBO Rep. 2012 Dec;13(12):1130-7. doi: 10.1038/embor.2012.161. Epub 2012 Oct 23.

DOI:10.1038/embor.2012.161
PMID:23090476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3513414/
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.

摘要

线粒体 DNA 复制的机制已经争论了十年。链置换模型表明，滞后链 DNA 合成是从轻链 DNA 复制原点（OriL）开始的，而链偶联模型则暗示 OriL 是可有可无的。哺乳动物的线粒体不能被转染，因此体内 OriL 的需求尚未得到解决。我们在这里使用体内饱和诱变来证明 OriL 对小鼠 mtDNA 的维持是必不可少的。生化和生物信息学分析表明，OriL 在脊椎动物中具有功能保守性。我们的发现强烈支持线粒体 DNA 复制的链置换模型。