You Changjun, Wang Yinsheng
Department of Chemistry, University of California , Riverside, California 92521-0403, United States.
Acc Chem Res. 2016 Feb 16;49(2):205-13. doi: 10.1021/acs.accounts.5b00437. Epub 2016 Jan 13.
The genetic integrity of living organisms is constantly threatened by environmental and endogenous sources of DNA damaging agents that can induce a plethora of chemically modified DNA lesions. Unrepaired DNA lesions may elicit cytotoxic and mutagenic effects and contribute to the development of human diseases including cancer and neurodegeneration. Understanding the deleterious outcomes of DNA damage necessitates the investigation about the effects of DNA adducts on the efficiency and fidelity of DNA replication and transcription. Conventional methods for measuring lesion-induced replicative or transcriptional alterations often require time-consuming colony screening and DNA sequencing procedures. Recently, a series of mass spectrometry (MS)-based strategies have been developed in our laboratory as an efficient platform for qualitative and quantitative analyses of the changes in genetic information induced by DNA adducts during DNA replication and transcription. During the past few years, we have successfully used these MS-based methods for assessing the replicative or transcriptional blocking and miscoding properties of more than 30 distinct DNA adducts. When combined with genetic manipulation, these methods have also been successfully employed for revealing the roles of various DNA repair proteins or translesion synthesis DNA polymerases (Pols) in modulating the adverse effects of DNA lesions on transcription or replication in mammalian and bacterial cells. For instance, we found that Escherichia coli Pol IV and its mammalian ortholog (i.e., Pol κ) are required for error-free bypass of N(2)-(1-carboxyethyl)-2'-deoxyguanosine (N(2)-CEdG) in cells. We also found that the N(2)-CEdG lesions strongly inhibit DNA transcription and they are repaired by transcription-coupled nucleotide excision repair in mammalian cells. In this Account, we focus on the development of MS-based approaches for determining the effects of DNA adducts on DNA replication and transcription, where liquid chromatography-tandem mass spectrometry is employed for the identification, and sometimes quantification, of the progeny products arising from the replication or transcription of lesion-bearing DNA substrates in vitro and in mammalian cells. We also highlight their applications to lesion bypass, mutagenesis, and repair studies of three representative types of DNA lesions, that is, the methylglyoxal-induced N(2)-CEdG, oxidatively induced 8,5'-cyclopurine-2'-deoxynucleosides, and regioisomeric alkylated thymidine lesions. Specially, we discuss the similar and distinct effects of the minor-groove DNA lesions including N(2)-CEdG and O(2)-alkylated thymidine lesions, as well as the major-groove O(4)-alkylated thymidine lesions on DNA replication and transcription machinery. For example, we found that the addition of an alkyl group to the O(4) position of thymine may facilitate its preferential pairing with guanine and thus induce exclusively the misincorporation of guanine nucleotide opposite the lesion, whereas alkylation of thymine at the O(2) position may render the nucleobase unfavorable in pairing with any of the canonical nucleobases and thus exhibit promiscuous miscoding properties during DNA replication and transcription. The MS-based strategies described herein should be generally applicable for quantitative measurement of the biological consequences and repair of other DNA lesions in vitro and in cells.
生物体的遗传完整性不断受到环境和内源性DNA损伤剂的威胁,这些损伤剂可诱导大量化学修饰的DNA损伤。未修复的DNA损伤可能引发细胞毒性和诱变效应,并导致包括癌症和神经退行性疾病在内的人类疾病的发展。要了解DNA损伤的有害后果,就必须研究DNA加合物对DNA复制和转录的效率及保真度的影响。传统的测量损伤诱导的复制或转录改变的方法通常需要耗时的菌落筛选和DNA测序程序。最近,我们实验室开发了一系列基于质谱(MS)的策略,作为一个高效平台,用于定性和定量分析DNA加合物在DNA复制和转录过程中诱导的遗传信息变化。在过去几年中,我们成功地使用这些基于MS的方法评估了30多种不同DNA加合物的复制或转录阻断及错配编码特性。当与基因操作相结合时,这些方法也已成功用于揭示各种DNA修复蛋白或跨损伤合成DNA聚合酶(Pols)在调节DNA损伤对哺乳动物和细菌细胞转录或复制的不利影响中的作用。例如,我们发现大肠杆菌Pol IV及其哺乳动物直系同源物(即Pol κ)是细胞中无错绕过N(2)-(1-羧乙基)-2'-脱氧鸟苷(N(2)-CEdG)所必需的。我们还发现N(2)-CEdG损伤强烈抑制DNA转录,并且它们在哺乳动物细胞中通过转录偶联核苷酸切除修复进行修复。在本综述中,我们重点介绍基于MS的方法的开发,用于确定DNA加合物对DNA复制和转录的影响,其中液相色谱-串联质谱用于鉴定,有时还用于定量体外和哺乳动物细胞中含损伤DNA底物复制或转录产生的子代产物。我们还强调了它们在三种代表性DNA损伤的损伤绕过、诱变和修复研究中的应用,即甲基乙二醛诱导的N(2)-CEdG、氧化诱导的8,5'-环嘌呤-2'-脱氧核苷以及区域异构体烷基化胸苷损伤。特别地,我们讨论了包括N(2)-CEdG和O(2)-烷基化胸苷损伤在内的小沟DNA损伤以及大沟O(4)-烷基化胸苷损伤对DNA复制和转录机制的相似和不同影响。例如,我们发现胸腺嘧啶O(4)位添加烷基可能促进其与鸟嘌呤的优先配对,从而仅诱导损伤对面鸟嘌呤核苷酸的错误掺入,而胸腺嘧啶O(2)位的烷基化可能使核碱基不利于与任何标准核碱基配对,因此在DNA复制和转录过程中表现出混杂的错配编码特性。本文所述的基于MS的策略通常应适用于体外和细胞中其他DNA损伤的生物学后果和修复的定量测量。