Evidence map›Paper›PMID 40250951›Full record

ArticleMethods in enzymology2025

Defining APOBEC-induced mutation signatures and modifying activities in yeast.

Tony M Mertz, Zachary W Kockler, Margo Coxon, Cameron Cordero, Atri K Raval, Alexander J Brown, Victoria Harcy, Dmitry A Gordenin, Steven A Roberts

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Methods in enzymology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  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
    Article
  2. Article
  3. Article
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

9 authors.

Tony M MertzDepartment of Microbiology and Molecular Genetics, University of Vermont Cancer Center, University of Vermont, Burlington, VT, United States.
Zachary W KocklerGenome Integrity & Structural Biology Laboratory, National Institute of Environmental Health Sciences, Durham, NC, United States.
Margo CoxonSchool of Molecular Biosciences, Washington State University, Pullman, WA, United States.
Cameron CorderoDepartment of Microbiology and Molecular Genetics, University of Vermont Cancer Center, University of Vermont, Burlington, VT, United States.
Atri K RavalDepartment of Microbiology and Molecular Genetics, University of Vermont Cancer Center, University of Vermont, Burlington, VT, United States.
Alexander J BrownSchool of Molecular Biosciences, Washington State University, Pullman, WA, United States.
Victoria HarcySchool of Molecular Biosciences, Washington State University, Pullman, WA, United States.
Dmitry A GordeninGenome Integrity & Structural Biology Laboratory, National Institute of Environmental Health Sciences, Durham, NC, United States.
Steven A RobertsDepartment of Microbiology and Molecular Genetics, University of Vermont Cancer Center, University of Vermont, Burlington, VT, United States. Electronic address: srober23@med.uvm.edu.

Funding

Mechanisms of genome instability induced by APOBEC Cytidine Deaminases & its impacts during cancer development - Diversity SupplementR01CA218112 · NCI · WASHINGTON STATE UNIVERSITY · PI ROBERTS, STEVEN A · 2017 to 2021
$2.2M
Regulation of APOBEC3 cytidine deaminase-induced mutation during cancerdevelopmentR01CA269784 · NCI · WASHINGTON STATE UNIVERSITY · PI STEVEN A ROBERTS · 2023 to 2026
$2.0M
NCI NIH HHS R01 CA218112NCI NIH HHS R01 CA269784
6 · The paper itself

Abstract

APOBEC cytidine deaminases guard cells in a variety of organisms from invading viruses and foreign nucleic acids. Recently, several human APOBECs have been implicated in mutating evolving cancer genomes. Expression of APOBEC3A and APOBEC3B in yeast allowed experimental derivation of the substitution patterns they cause in dividing cells, which provided critical links to these enzymes in the etiology of the COSMIC single base substitution (SBS) signatures 2 and 13 in human tumors. Additionally, the ability to scale yeast experiments to high-throughput screens allows use of this system to also investigate cellular pathways impacting the frequency of APOBEC-induced mutation. Here, we present validated methods utilizing yeast to determine APOBEC mutation signatures, genetic interactors, and chromosomal substrate preferences. These methods can be employed to assess the potential of other human APOBECs and APOBEC orthologs in different species to contribute to cancer genome evolution as well as define the pathways that protect the nuclear genome from inadvertent APOBEC activity during viral restriction.

Indexed as

APOBEC DeaminasesCytidine DeaminaseMutationSaccharomyces cerevisiaeHumansMinor Histocompatibility AntigensProteinsAPOBEC3A protein, humanAPOBEC3B protein, humanAPOBEC DeaminasesCytidine DeaminaseMinor Histocompatibility AntigensProteinsAmplicon sequencingAPOBEC cytidine deaminasesCancerHigh-throughput screenMutagenesisMutation signatureSBS13SBS2Whole genome sequencingYeast

Identifiers

PMID40250951
PMCPMC12324072

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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.