ArticlebioRxiv : the preprint server for biology2025
Elevated mutation near crossovers inhibits the evolution of recombination.
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.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
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
Identifiers
What Socratic holds
Registered trials
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.