Evidence map›Paper›PMID 28334887›Full record

ArticleNucleic acids research2017

Avoidance of APOBEC3B-induced mutation by error-free lesion bypass.

James I Hoopes, Amber L Hughes, Lauren A Hobson, Luis M Cortez, Alexander J Brown, Steven A Roberts

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 34 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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  4. APOBEC3A deaminates CTG hairpin loops to promote fragility and instability of expanded CAG/CTG repeats.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. Investigation of Break-Induced Replication in Yeast.Methods in molecular biology (Clifton, N.J.) · 2021
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  18. Review
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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

6 authors at 1 institution in 1 country.

James I HoopesSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Amber L HughesSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Lauren A HobsonSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Luis M CortezSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Alexander J BrownSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Steven A RobertsSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA.
Washington State University · US

Funding

TRAINING IN BIOTECHNOLOGY: EMPHASIS ON PROTEIN CHEMISTRYT32GM008336 · NIGMS · WASHINGTON STATE UNIVERSITY · PI CALL, DOUGLAS R. · 1989 to 2023
$8.9M
Environmentally-modulated cytosine deamination in genome instability and cancerR00ES022633 · NIEHS · WASHINGTON STATE UNIVERSITY · PI ROBERTS, STEVEN A · 2015 to 2017
$868k
NIEHS NIH HHS R00 ES022633NIGMS NIH HHS T32 GM008336
6 · The paper itself

Abstract

APOBEC cytidine deaminases mutate cancer genomes by converting cytidines into uridines within ssDNA during replication. Although uracil DNA glycosylases limit APOBEC-induced mutation, it is unknown if subsequent base excision repair (BER) steps function on replication-associated ssDNA. Hence, we measured APOBEC3B-induced CAN1 mutation frequencies in yeast deficient in BER endonucleases or DNA damage tolerance proteins. Strains lacking Apn1, Apn2, Ntg1, Ntg2 or Rev3 displayed wild-type frequencies of APOBEC3B-induced canavanine resistance (CanR). However, strains without error-free lesion bypass proteins Ubc13, Mms2 and Mph1 displayed respective 4.9-, 2.8- and 7.8-fold higher frequency of APOBEC3B-induced CanR. These results indicate that mutations resulting from APOBEC activity are avoided by deoxyuridine conversion to abasic sites ahead of nascent lagging strand DNA synthesis and subsequent bypass by error-free template switching. We found this mechanism also functions during telomere re-synthesis, but with a diminished requirement for Ubc13. Interestingly, reduction of G to C substitutions in Ubc13-deficient strains uncovered a previously unknown role of Ubc13 in controlling the activity of the translesion synthesis polymerase, Rev1. Our results highlight a novel mechanism for error-free bypass of deoxyuridines generated within ssDNA and suggest that the APOBEC mutation signature observed in cancer genomes may under-represent the genomic damage these enzymes induce.

Indexed as

DNA DamageDNA RepairCytidine DeaminaseDNA ReplicationGenes, ReporterModels, BiologicalMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCytidine DeaminaseSaccharomyces cerevisiae Proteins

Identifiers

PMID28334887
PMCPMC5605239
OpenAlexW2592429281

What OpenQuestion holds

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LicenceCC BY-NC
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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.