Evidence map›Paper›PMID 33848333›Full record

ArticleGenetics2021

Multiplexing mutation rate assessment: determining pathogenicity of Msh2 variants in Saccharomyces cerevisiae.

Anja R Ollodart, Chiann-Ling C Yeh, Aaron W Miller, Brian H Shirts, Adam S Gordon, Maitreya J Dunham

Abstract readValidation Study
In one paragraph

Article in Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. The power of many: when genetics met yeasts and high-throughput.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. RosettaDDGPrediction for high-throughput mutational scans: From stability to binding.Protein science : a publication of the Protein Society · 2023
    Article
  9. Review
  10. Article
  11. 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

6 authors.

Anja R OllodartMolecular Cellular Biology Program, University of Washington, Seattle, WA 98195, USA.ORCID 0000-0002-6329-9463
Chiann-Ling C YehGenome Sciences Department, University of Washington, Seattle, WA 98195, USA.ORCID 0000-0003-4032-8871
Aaron W MillerGenome Sciences Department, University of Washington, Seattle, WA 98195, USA.
Brian H ShirtsDepartment of Laboratory Medicine, University of Washington, Seattle, WA 98195, USA.ORCID 0000-0002-7188-6764
Adam S GordonDepartment of Pharmacology, Northwestern University, Chicago, IL 60208, USA.ORCID 0000-0002-2058-7289
Maitreya J DunhamGenome Sciences Department, University of Washington, Seattle, WA 98195, USA.ORCID 0000-0001-9944-2666

Funding

INTERDISCIPLINARY TRAINING IN GENOMIC SCIENCEST32HG000035 · NHGRI · UNIVERSITY OF WASHINGTON · PI Bruce Colston Trapnell · 1995 to 2026
$24.2M
TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI YATES III, JOHN R · 2012 to 2021
$20.7M
Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
NCI NIH HHS T32 CA080416NHGRI NIH HHS T32 HG000035NIGMS NIH HHS P41 GM103533
6 · The paper itself

Abstract

Despite the fundamental importance of mutation rate as a driving force in evolution and disease risk, common methods to assay mutation rate are time-consuming and tedious. Established methods such as fluctuation tests and mutation accumulation experiments are low-throughput and often require significant optimization to ensure accuracy. We established a new method to determine the mutation rate of many strains simultaneously by tracking mutation events in a chemostat continuous culture device and applying deep sequencing to link mutations to alleles of a DNA-repair gene. We applied this method to assay the mutation rate of hundreds of Saccharomyces cerevisiae strains carrying mutations in the gene encoding Msh2, a DNA repair enzyme in the mismatch repair pathway. Loss-of-function mutations in MSH2 are associated with hereditary nonpolyposis colorectal cancer, an inherited disorder that increases risk for many different cancers. However, the vast majority of MSH2 variants found in human populations have insufficient evidence to be classified as either pathogenic or benign. We first benchmarked our method against Luria-Delbrück fluctuation tests using a collection of published MSH2 missense variants. Our pooled screen successfully identified previously characterized nonfunctional alleles as high mutators. We then created an additional 185 human missense variants in the yeast ortholog, including both characterized and uncharacterized alleles curated from ClinVar and other clinical testing data. In a set of alleles of known pathogenicity, our assay recapitulated ClinVar's classification; we then estimated pathogenicity for 157 variants classified as uncertain or conflicting reports of significance. This method is capable of studying the mutation rate of many microbial species and can be applied to problems ranging from the generation of high-fidelity polymerases to measuring the frequency of antibiotic resistance emergence.

Indexed as

DNA, FungalDNA Mutational AnalysisDrug Resistance, MicrobialGene LibraryHigh-Throughput Screening AssaysHumansMutation, MissenseMutation RateMutS Homolog 2 ProteinSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA, FungalMSH2 protein, humanMSH2 protein, S cerevisiaeMutS Homolog 2 ProteinSaccharomyces cerevisiae ProteinschemostatMSH2mutation rateyeast

Identifiers

PMID33848333
PMCPMC8225350

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Registered trials

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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.