Suppr超能文献

DNA断裂代谢的质量控制:最终,这是件好事。

Quality control of DNA break metabolism: in the 'end', it's a good thing.

作者信息

Kanaar Roland, Wyman Claire, Rothstein Rodney

机构信息

Department of Cell Biology and Genetics, Erasmus Medical Center, Rotterdam, The Netherlands.

出版信息

EMBO J. 2008 Feb 20;27(4):581-8. doi: 10.1038/emboj.2008.11.

Abstract

DNA ends pose specific problems in the control of genetic information quality. Ends of broken DNA need to be rejoined to avoid genome rearrangements, whereas natural DNA ends of linear chromosomes, telomeres, need to be stable and hidden from the DNA damage response. Efficient DNA end metabolism, either at induced DNA breaks or telomeres, does not result from the machine-like precision of molecular reactions, but rather from messier, more stochastic processes. The necessary molecular interactions are dynamically unstable, with constructive and destructive processes occurring in competition. In the end, quality control comes from the constant building up and tearing down of inappropriate, but also appropriate reaction steps in combination with factors that only slightly shift the equilibrium to eventually favour appropriate events. Thus, paradoxically, enzymes antagonizing DNA end metabolism help to ensure that genome maintenance becomes a robust process.

摘要

DNA末端在遗传信息质量控制方面存在特定问题。断裂DNA的末端需要重新连接以避免基因组重排,而线性染色体的天然DNA末端,即端粒,需要保持稳定并免受DNA损伤反应的影响。无论是在诱导的DNA断裂处还是端粒处,高效的DNA末端代谢并非源于分子反应如机器般的精确性,而是源于更混乱、更具随机性的过程。必要的分子相互作用是动态不稳定的,建设性和破坏性过程相互竞争。最终,质量控制来自于不断地构建和拆解不适当但也包括适当的反应步骤,以及一些仅轻微改变平衡以最终有利于适当事件的因素。因此,矛盾的是,拮抗DNA末端代谢的酶有助于确保基因组维护成为一个稳健的过程。

相似文献

1
Quality control of DNA break metabolism: in the 'end', it's a good thing.
EMBO J. 2008 Feb 20;27(4):581-8. doi: 10.1038/emboj.2008.11.
2
Nuclear organization in DNA end processing: Telomeres vs double-strand breaks.
DNA Repair (Amst). 2015 Aug;32:134-140. doi: 10.1016/j.dnarep.2015.04.024. Epub 2015 May 1.
3
The role of the nonhomologous end-joining DNA double-strand break repair pathway in telomere biology.
Annu Rev Genet. 2006;40:237-77. doi: 10.1146/annurev.genet.39.110304.095755.
4
Recombination proteins and telomere stability in plants.
Curr Protein Pept Sci. 2011 Mar;12(2):84-92. doi: 10.2174/138920311795684931.
5
Mdt1 facilitates efficient repair of blocked DNA double-strand breaks and recombinational maintenance of telomeres.
Mol Cell Biol. 2007 Sep;27(18):6532-45. doi: 10.1128/MCB.00471-07. Epub 2007 Jul 16.
6
DNA damage response at functional and dysfunctional telomeres.
Genes Dev. 2008 Jan 15;22(2):125-40. doi: 10.1101/gad.1626908.
7
The Response to DNA Damage at Telomeric Repeats and Its Consequences for Telomere Function.
Genes (Basel). 2019 Apr 24;10(4):318. doi: 10.3390/genes10040318.
8
Telomeres and double-strand breaks - all's well that "ends" well. ..
Radiat Res. 2008 Jan;169(1):1-7. doi: 10.1667/RR1197.1.
9
Telomeres and the DNA damage response: why the fox is guarding the henhouse.
DNA Repair (Amst). 2004 Aug-Sep;3(8-9):979-88. doi: 10.1016/j.dnarep.2004.05.009.

引用本文的文献

1
CRISPR-Based Gene Therapies: From Preclinical to Clinical Treatments.
Cells. 2024 May 8;13(10):800. doi: 10.3390/cells13100800.
2
The landscape of aging.
Sci China Life Sci. 2022 Dec;65(12):2354-2454. doi: 10.1007/s11427-022-2161-3. Epub 2022 Sep 2.
3
Epigenetic Clock and Circadian Rhythms in Stem Cell Aging and Rejuvenation.
J Pers Med. 2021 Oct 20;11(11):1050. doi: 10.3390/jpm11111050.
4
DNA Double Strand Break Repair Pathways in Response to Different Types of Ionizing Radiation.
Front Genet. 2021 Sep 30;12:738230. doi: 10.3389/fgene.2021.738230. eCollection 2021.
5
Crosstalk between autophagy and DNA repair systems.
Turk J Biol. 2021 Jun 23;45(3):235-252. doi: 10.3906/biy-2103-51. eCollection 2021.
6
New answers to the old RIDDLE: RNF168 and the DNA damage response pathway.
FEBS J. 2022 May;289(9):2467-2480. doi: 10.1111/febs.15857. Epub 2021 Apr 16.
7
Opportunities and Challenges in Stem Cell Aging.
Adv Exp Med Biol. 2021;1341:143-175. doi: 10.1007/5584_2021_624.
8
Aging: A cell source limiting factor in tissue engineering.
World J Stem Cells. 2019 Oct 26;11(10):787-802. doi: 10.4252/wjsc.v11.i10.787.
9
The functional importance of lamins, actin, myosin, spectrin and the LINC complex in DNA repair.
Exp Biol Med (Maywood). 2019 Nov;244(15):1382-1406. doi: 10.1177/1535370219876651. Epub 2019 Oct 4.
10
Dynamic Processing of Displacement Loops during Recombinational DNA Repair.
Mol Cell. 2019 Mar 21;73(6):1255-1266.e4. doi: 10.1016/j.molcel.2019.01.005. Epub 2019 Feb 5.

本文引用的文献

1
Differential regulation of the cellular response to DNA double-strand breaks in G1.
Mol Cell. 2008 Apr 11;30(1):73-85. doi: 10.1016/j.molcel.2008.01.016.
2
Ku recruits XLF to DNA double-strand breaks.
EMBO Rep. 2008 Jan;9(1):91-6. doi: 10.1038/sj.embor.7401137. Epub 2007 Dec 7.
5
Ctp1/CtIP and the MRN complex collaborate in the initial steps of homologous recombination.
Mol Cell. 2007 Nov 9;28(3):351-2. doi: 10.1016/j.molcel.2007.10.016.
6
Human CtIP promotes DNA end resection.
Nature. 2007 Nov 22;450(7169):509-14. doi: 10.1038/nature06337. Epub 2007 Oct 28.
7
Real-time measurements of the nucleation, growth and dissociation of single Rad51-DNA nucleoprotein filaments.
Nucleic Acids Res. 2007;35(21):7171-87. doi: 10.1093/nar/gkm752. Epub 2007 Oct 18.
9
The structure-specific endonuclease Mus81 contributes to replication restart by generating double-strand DNA breaks.
Nat Struct Mol Biol. 2007 Nov;14(11):1096-104. doi: 10.1038/nsmb1313. Epub 2007 Oct 14.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验