Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA.
Gene Bridges GmbH, Im Neuenheimer Feld 584, 69120 Heidelberg, Germany.
Mutat Res. 2014 Mar;761:21-33. doi: 10.1016/j.mrfmmm.2014.01.005. Epub 2014 Feb 1.
Low fidelity Escherichia coli DNA polymerase V (pol V/UmuD'2C) is best characterized for its ability to perform translesion synthesis (TLS). However, in recA730 lexA(Def) strains, the enzyme is expressed under optimal conditions allowing it to compete with the cell's replicase for access to undamaged chromosomal DNA and leads to a substantial increase in spontaneous mutagenesis. We have recently shown that a Y11A substitution in the "steric gate" residue of UmuC reduces both base and sugar selectivity of pol V, but instead of generating an increased number of spontaneous mutations, strains expressing umuC_Y11A are poorly mutable in vivo. This phenotype is attributed to efficient RNase HII-initiated repair of the misincorporated ribonucleotides that concomitantly removes adjacent misincorporated deoxyribonucleotides. We have utilized the ability of the pol V steric gate mutant to promote incorporation of large numbers of errant ribonucleotides into the E. coli genome to investigate the fundamental mechanisms underlying ribonucleotide excision repair (RER). Here, we demonstrate that RER is normally facilitated by DNA polymerase I (pol I) via classical "nick translation". In vitro, pol I displaces 1-3 nucleotides of the RNA/DNA hybrid and through its 5'→3' (exo/endo) nuclease activity releases ribo- and deoxyribonucleotides from DNA. In vivo, umuC_Y11A-dependent mutagenesis changes significantly in polymerase-deficient, or proofreading-deficient polA strains, indicating a pivotal role for pol I in ribonucleotide excision repair (RER). However, there is also considerable redundancy in the RER pathway in E. coli. Pol I's strand displacement and FLAP-exo/endonuclease activities can be facilitated by alternate enzymes, while the DNA polymerization step can be assumed by high-fidelity pol III. We conclude that RNase HII and pol I normally act to minimize the genomic instability that is generated through errant ribonucleotide incorporation, but that the "nick-translation" activities encoded by the single pol I polypeptide can be undertaken by a variety of back-up enzymes.
低保真大肠杆菌 DNA 聚合酶 V(pol V/UmuD'2C)以其进行跨损伤合成(TLS)的能力而被最好地描述。然而,在 recA730 lexA(Def)菌株中,该酶在最佳条件下表达,使其能够与细胞的复制酶竞争对未受损染色体 DNA 的访问,并导致自发突变率大幅增加。我们最近表明,UmuC 中的“空间位阻门”残基的 Y11A 取代降低了 pol V 的碱基和糖选择性,但没有产生更多的自发突变,表达 umuC_Y11A 的菌株在体内的突变能力很差。这种表型归因于错误掺入的核糖核苷酸的 RNase HII 起始修复,同时去除相邻错误掺入的脱氧核糖核苷酸。我们利用 pol V 空间位阻突变体将大量错误掺入的核糖核苷酸掺入大肠杆菌基因组的能力来研究核糖核苷酸切除修复(RER)的基本机制。在这里,我们证明 RER 通常由 DNA 聚合酶 I(pol I)通过经典的“缺口平移”来促进。在体外,pol I 置换 RNA/DNA 杂交体的 1-3 个核苷酸,并通过其 5'→3'(外切/内切)核酸酶活性从 DNA 中释放核糖核苷酸和脱氧核糖核苷酸。在体内,umuC_Y11A 依赖性诱变在聚合酶缺陷或校对缺陷的 polA 菌株中发生显著变化,表明 pol I 在核糖核苷酸切除修复(RER)中起着关键作用。然而,大肠杆菌中 RER 途径也存在相当大的冗余。pol I 的链置换和 FLAP-外切/内切核酸酶活性可以由替代酶促进,而 DNA 聚合步骤可以由高保真 pol III 承担。我们得出结论,RNase HII 和 pol I 通常会最大限度地减少因错误掺入核糖核苷酸而产生的基因组不稳定性,但单个 pol I 多肽编码的“缺口平移”活性可以由多种备用酶来完成。