Evidence map›Paper›PMID 23988736›Full record

ArticleDNA repair2013

The choice of nucleotide inserted opposite abasic sites formed within chromosomal DNA reveals the polymerase activities participating in translesion DNA synthesis.

Kin Chan, Michael A Resnick, Dmitry A Gordenin

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 83 citations in OpenAlex.

  1. Distinct repair processes produce APOBEC-induced deletions, tandem substitutions, and complex mutations in yeast and human cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  12. The Catalytic Activity of Human REV1 on Undamaged and Damaged DNA.International journal of molecular sciences · 2024
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  16. Human APOBEC3B promotes tumor heterogeneitybioRxiv : the preprint server for biology · 2023
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  19. Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Kin ChanChromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA. Electronic address: chank2@niehs.nih.gov.
Michael A Resnick
Dmitry A Gordenin
National Institutes of Health · USNational Institute of Environmental Health Sciences · US

Funding

MOLECULAR MECHANISMS OF DNA REPAIR AND RECOMBINATION IN YEASTZ01ES065073 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1991 to 2008
$2.8M
Intramural NIH HHS Z01 ES065073Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Abasic sites in genomic DNA can be a significant source of mutagenesis in biological systems, including human cancers. Such mutagenesis requires translesion DNA synthesis (TLS) bypass of the abasic site by specialized DNA polymerases. The abasic site bypass specificity of TLS proteins had been studied by multiple means in vivo and in vitro, although the generality of the conclusions reached have been uncertain. Here, we introduce a set of yeast reporter strains for investigating the in vivo specificity of abasic site bypass at numerous random positions within chromosomal DNA. When shifted to 37°C, these strains underwent telomere uncapping and resection that exposed reporter genes within a long 3' ssDNA overhang. Human APOBEC3G cytosine deaminase was expressed to create uracils in ssDNA, which were excised by uracil-DNA N-glycosylase. During repair synthesis, error-prone TLS bypassed the resulting abasic sites. Because of APOBEC3G's strict motif specificity and the restriction of abasic site formation to only one DNA strand, this system provides complete information about the location of abasic sites that led to mutations. We recapitulated previous findings on the roles of REV1 and REV3. Further, we found that sequence context can strongly influence the relative frequency of A or C insertion. We also found that deletion of Pol32, a non-essential common subunit of Pols δ and ζ, resulted in residual low-frequency C insertion dependent on Rev1 catalysis. We summarize our results in a detailed model of the interplay between TLS components leading to error-prone bypass of abasic sites. Our results underscore the utility of this system for studying TLS bypass of many types of lesions within genomic DNA.

Indexed as

Chromosomes, FungalAPOBEC-3G DeaminaseCytidine DeaminaseDNA DamageDNA-Directed DNA PolymeraseDNA, FungalDNA RepairDNA, Single-StrandedHumansMutagenesis, InsertionalNucleotidesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsUracilUracil-DNA GlycosidaseAPOBEC-3G DeaminaseAPOBEC3G protein, humanCytidine DeaminaseDNA-Directed DNA PolymeraseDNA, FungalDNA, Single-StrandedNucleotidesSaccharomyces cerevisiae ProteinsUracilUracil-DNA GlycosidaseAbasic siteAPOBECDeoxycytidyltransferaseSingle-strand DNATranslesion DNA synthesis

Identifiers

PMID23988736
PMCPMC3825800
OpenAlexW2094773814

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.