scholarly journals Identification of an Unfolding Intermediate for a DNA Lesion Bypass Polymerase

2012 ◽  
Vol 25 (7) ◽  
pp. 1531-1540 ◽  
Author(s):  
Shanen M. Sherrer ◽  
Brian A. Maxwell ◽  
Lindsey R. Pack ◽  
Kevin A. Fiala ◽  
Jason D. Fowler ◽  
...  
Keyword(s):  
Lesion Bypass ◽  
Dna Lesion ◽  
Bypass Polymerase

Determination of DNA lesion bypass using a ChIP-based assay

DNA Repair ◽  
2021 ◽  
pp. 103230
Author(s):  
Dayong Wu ◽  
Ananya Banerjee ◽  
Shurui Cai ◽  
Na Li ◽  
Chunhua Han ◽  
...  
Keyword(s):  
Lesion Bypass ◽  
Dna Lesion

scholarly journals Advances in Structural and Single-Molecule Methods for Investigating DNA Lesion Bypass and Repair Polymerases

2016 ◽  
Vol 30 (1) ◽  
pp. 260-269 ◽  
Author(s):  
Austin T. Raper ◽  
Andrew J. Reed ◽  
Varun V. Gadkari ◽  
Zucai Suo
Keyword(s):  
Single Molecule ◽  
Lesion Bypass ◽  
Dna Lesion

Use of yeast transformation by oligonucleotides to study DNA lesion bypass in vivo

2002 ◽  
Vol 502 (1-2) ◽  
pp. 53-60 ◽  
Author(s):  
Chie Otsuka ◽  
Keita Kobayashi ◽  
Naho Kawaguchi ◽  
Nozomu Kunitomi ◽  
Kei Moriyama ◽  
...  
Keyword(s):  
Yeast Transformation ◽  
Lesion Bypass ◽  
Dna Lesion

scholarly journals Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication

2017 ◽  
Vol 114 (11) ◽  
pp. E2205-E2214 ◽  
Author(s):  
Shih-Hsun Hung ◽  
Ronald P. Wong ◽  
Helle D. Ulrich ◽  
Cheng-Fu Kao
Keyword(s):  
Dna Damage ◽  
Replication Fork ◽  
Dna Lesions ◽  
Template Switching ◽  
Lesion Bypass ◽  
Dna Damage Tolerance ◽  
Cytological Evidence ◽  
Histone H2b ◽  
Chromatin Dynamics ◽  
Dna Lesion

DNA lesion bypass is mediated by DNA damage tolerance (DDT) pathways and homologous recombination (HR). The DDT pathways, which involve translesion synthesis and template switching (TS), are activated by the ubiquitylation (ub) of PCNA through components of the RAD6-RAD18 pathway, whereas the HR pathway is independent of RAD18. However, it is unclear how these processes are coordinated within the context of chromatin. Here we show that Bre1, an ubiquitin ligase specific for histone H2B, is recruited to chromatin in a manner coupled to replication of damaged DNA. In the absence of Bre1 or H2Bub, cells exhibit accumulation of unrepaired DNA lesions. Consequently, the damaged forks become unstable and resistant to repair. We provide physical, genetic, and cytological evidence that H2Bub contributes toward both Rad18-dependent TS and replication fork repair by HR. Using an inducible system of DNA damage bypass, we further show that H2Bub is required for the regulation of DDT after genome duplication. We propose that Bre1-H2Bub facilitates fork recovery and gap-filling repair by controlling chromatin dynamics in response to replicative DNA damage.

scholarly journals The Mutational Specificity of the Dbh Lesion Bypass Polymerase and Its Implications

2002 ◽  
Vol 277 (31) ◽  
pp. 28157-28166 ◽  
Author(s):  
Olga Potapova ◽  
Nigel D. F. Grindley ◽  
Catherine M. Joyce
Keyword(s):  
Lesion Bypass ◽  
Mutational Specificity ◽  
Bypass Polymerase

scholarly journals An underlying mechanism for the increased mutagenesis of lagging-strand genes inBacillus subtilis

2015 ◽  
Vol 112 (10) ◽  
pp. E1096-E1105 ◽  
Author(s):  
Samuel Million-Weaver ◽  
Ariana N. Samadpour ◽  
Daniela A. Moreno-Habel ◽  
Patrick Nugent ◽  
Mitchell J. Brittnacher ◽  
...  
Keyword(s):  
Excision Repair ◽  
Underlying Mechanism ◽  
Mutation Rates ◽  
Dependent Manner ◽  
Lesion Bypass ◽  
Dna Lesion ◽  
Accelerated Evolution ◽  
Recombination Protein ◽  
Y Family ◽  
Lagging Strand

We previously reported that lagging-strand genes accumulate mutations faster than those encoded on the leading strand inBacillus subtilis. Although we proposed that orientation-specific encounters between replication and transcription underlie this phenomenon, the mechanism leading to the increased mutagenesis of lagging-strand genes remained unknown. Here, we report that the transcription-dependent and orientation-specific differences in mutation rates of genes require theB. subtilisY-family polymerase, PolY1 (yqjH). We find that without PolY1, association of the replicative helicase, DnaC, and the recombination protein, RecA, with lagging-strand genes increases in a transcription-dependent manner. These data suggest that PolY1 promotes efficient replisome progression through lagging-strand genes, thereby reducing potentially detrimental breaks and single-stranded DNA at these loci. Y-family polymerases can alleviate potential obstacles to replisome progression by facilitating DNA lesion bypass, extension of D-loops, or excision repair. We find that the nucleotide excision repair (NER) proteins UvrA, UvrB, and UvrC, but not RecA, are required for transcription-dependent asymmetry in mutation rates of genes in the two orientations. Furthermore, we find that the transcription-coupling repair factor Mfd functions in the same pathway as PolY1 and is also required for increased mutagenesis of lagging-strand genes. Experimental and SNP analyses ofB. subtilisgenomes show mutational footprints consistent with these findings. We propose that the interplay between replication and transcription increases lesion susceptibility of, specifically, lagging-strand genes, activating an Mfd-dependent error-prone NER mechanism. We propose that this process, at least partially, underlies the accelerated evolution of lagging-strand genes.

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