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本文引用的文献

1
Replication of ribonucleotide-containing DNA templates by yeast replicative polymerases.酵母复制聚合酶对含核苷酸 DNA 模板的复制。
DNA Repair (Amst). 2011 Aug 15;10(8):897-902. doi: 10.1016/j.dnarep.2011.05.009. Epub 2011 Jun 23.
2
Mutagenic processing of ribonucleotides in DNA by yeast topoisomerase I.酵母拓扑异构酶 I 对 DNA 中核糖核苷酸的诱变处理。
Science. 2011 Jun 24;332(6037):1561-4. doi: 10.1126/science.1205016.
3
Mismatch repair-independent tandem repeat sequence instability resulting from ribonucleotide incorporation by DNA polymerase ε.DNA 聚合酶 ε 通过核苷酸掺入导致的错配修复非依赖性串联重复序列不稳定。
DNA Repair (Amst). 2011 May 5;10(5):476-82. doi: 10.1016/j.dnarep.2011.02.001. Epub 2011 Mar 16.
4
CAF-I-dependent control of degradation of the discontinuous strands during mismatch repair.CAF-I 依赖性控制错配修复过程中不连续链的降解。
Proc Natl Acad Sci U S A. 2011 Feb 15;108(7):2753-8. doi: 10.1073/pnas.1015914108. Epub 2011 Jan 31.
5
Differential correction of lagging-strand replication errors made by DNA polymerases {alpha} and {delta}.滞后链复制错误的差异校正,由 DNA 聚合酶α和δ造成。
Proc Natl Acad Sci U S A. 2010 Dec 7;107(49):21070-5. doi: 10.1073/pnas.1013048107. Epub 2010 Nov 1.
6
The high fidelity and unique error signature of human DNA polymerase epsilon.人类 DNA 聚合酶 ε 的高保真度和独特的错误特征。
Nucleic Acids Res. 2011 Mar;39(5):1763-73. doi: 10.1093/nar/gkq1034. Epub 2010 Oct 29.
7
Mechanisms of mutagenesis in vivo due to imbalanced dNTP pools.体内由于不平衡的 dNTP 池引起的诱变机制。
Nucleic Acids Res. 2011 Mar;39(4):1360-71. doi: 10.1093/nar/gkq829. Epub 2010 Oct 20.
8
Genome-wide model for the normal eukaryotic DNA replication fork.全基因组模型研究正常真核生物 DNA 复制叉。
Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17674-9. doi: 10.1073/pnas.1010178107. Epub 2010 Sep 27.
9
Genome instability due to ribonucleotide incorporation into DNA.由于核苷酸掺入 DNA 而导致的基因组不稳定。
Nat Chem Biol. 2010 Oct;6(10):774-81. doi: 10.1038/nchembio.424. Epub 2010 Aug 22.
10
Visualizing one-dimensional diffusion of eukaryotic DNA repair factors along a chromatin lattice.可视化真核 DNA 修复因子沿着染色质格子的一维扩散。
Nat Struct Mol Biol. 2010 Aug;17(8):932-8. doi: 10.1038/nsmb.1858. Epub 2010 Jul 25.

平衡真核复制的不对称性与复制保真度。

Balancing eukaryotic replication asymmetry with replication fidelity.

机构信息

Laboratory of Molecular Genetics and Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709, USA.

出版信息

Curr Opin Chem Biol. 2011 Oct;15(5):620-6. doi: 10.1016/j.cbpa.2011.07.025. Epub 2011 Aug 19.

DOI:10.1016/j.cbpa.2011.07.025
PMID:21862387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3189284/
Abstract

Coordinated replication of eukaryotic nuclear genomes is asymmetric, with copying of a leading strand template preceding discontinuous copying of the lagging strand template. Replication is catalyzed by DNA polymerases α, δ and ɛ, enzymes that are related yet differ in physical and biochemical properties, including fidelity. Recent studies suggest that Pol ɛ is normally the primary leading strand replicase, whereas most synthesis by Pol δ occurs during lagging strand replication. New studies show that replication asymmetry can generate strand-specific genome instability resulting from biased deoxynucleotide pools and unrepaired ribonucleotides incorporated into DNA during replication, and that the eukaryotic replication machinery has evolved to most efficiently correct those replication errors that are made at the highest rates.

摘要

真核生物核基因组的复制是不对称的,先导链模板的复制先于滞后链模板的不连续复制。复制由 DNA 聚合酶 α、δ 和 ε 催化,这些酶虽然相关,但在物理和生化性质上存在差异,包括保真度。最近的研究表明,Pol ɛ 通常是主要的先导链复制酶,而 Pol δ 的大部分合成发生在滞后链复制过程中。新的研究表明,复制不对称性会导致由脱氧核苷酸池偏倚和复制过程中未修复的核糖核苷酸掺入 DNA 引起的链特异性基因组不稳定性,并且真核复制机制已经进化到能够最有效地纠正那些以最高速率发生的复制错误。