Evidence map›Paper›PMID 41279728›Full record

ArticlebioRxiv : the preprint server for biology2025

Elevated mutation near crossovers inhibits the evolution of recombination.

Bret A Payseur, Sarah P Otto

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Bret A PayseurLaboratory of Genetics, University of Wisconsin-Madison, Madison, Wisconsin, U. S. A.ORCID 0000-0003-3109-4778
Sarah P OttoDepartment of Zoology and Biodiversity Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.ORCID 0000-0003-3042-0818

Funding

Evolution of Phenotypic Extremes: Genetic Determinants of Gigantism, Boldness, and RecombinationR35GM139412 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI Bret A. Payseur · 2021 to 2026
$5.7M
NIGMS NIH HHS R35 GM139412
6 · The paper itself

Abstract

Recombination diversifies offspring genomes and helps ensure chromosome segregation during meiosis. Mutation rates are elevated near crossovers due to the induction of double-strand breaks and their imperfect repair, a byproduct of recombination typically ignored by theory designed to explain its evolution. To examine the evolutionary role of mutagenic recombination, we analyze a population genetic model in which a modifier locus controls both the rate of recombination between two loci experiencing viability selection and the rate of mutation at those loci. Analytical and numerical results demonstrate that the advantage of recombination conferred by its capacity to remove epistatic, deleterious variants is overcome by the selective cost of even small increases in the mutation rate. By incorporating the mutagenic effects of recombination, our analysis extends a rich body of theory to acknowledge a molecular feature inherent in the formation of crossovers. Our findings suggest that higher recombination rate evolves by altering steps in the crossover pathway that are less likely to inflict mutational damage.

Indexed as

deleterious mutationDNA repairdouble-strand breakepistasisrecombination

Identifiers

PMID41279728
PMCPMC12636366

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.