Evidence map›Paper›PMID 31932974›Full record

ArticleCurrent genetics2020

Timing of appearance of new mutations during yeast meiosis and their association with recombination.

Osama Mansour, Liat Morciano, Keren Zion, Renana Elgrabli, Drora Zenvirth, Giora Simchen, Ayelet Arbel-Eden

Abstract read
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Article in Current genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Mutations and structural variants arising during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Practical Approaches for the YeastInternational journal of molecular sciences · 2023
    Review
  6. Chromosome-dependent aneuploid formation in Spo11-less meiosis.Genes to cells : devoted to molecular & cellular mechanisms · 2023
    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

7 authors.

Osama MansourDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel.
Liat MorcianoDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel.
Keren ZionDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel.
Renana ElgrabliDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel.
Drora ZenvirthDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel.
Giora SimchenDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel. giora.simchen@mail.huji.ac.il.
Ayelet Arbel-EdenDepartment of Genetics, Hebrew University of Jerusalem, 91904, Jerusalem, Israel. ayeletar@hac.ac.il.ORCID http://orcid.org/0000-0001-6630-0805

Funding

Israel Science Foundation 501/16United States - Israel Binational Science Foundation #2009299
6 · The paper itself

Abstract

Mutations in budding yeast occur in meiosis at higher frequencies than in cells grown vegetatively. In contrast to mutations that occur in somatic cells, meiotic mutations have a special, long-range impact on evolution, because they are transferred to the following generations through the gametes. Understanding the mechanistic basis of meiotic mutagenicity is still lacking, however. Here, we report studies of mutagenicity in the reporter gene CAN1, in which forward mutation events in meiosis are sevenfold higher than in mitotic cells, as determined by fluctuation analysis. Meiotic mutations appear approximately at the same time as heteroallelic-recombination products and as meiotic DSBs. Recombination-associated timing of meiotic mutagenicity is further augmented by the absence of meiotic mutations in cells arrested after pre-meiotic DNA synthesis. More than 40% of the mutations generated in meiosis in CAN1 are found on chromosomes that have recombined in the 2.2 kb covering the reporter, implying that the mutations have resulted from recombination events and that meiotic recombination is mutagenic. The induced expression in yeast meiosis of low-fidelity DNA polymerases coded by the genes REV1, REV3, RAD30, and POL4 makes them attractive candidates for introducing mutations. However, in our extensive experiments with polymerase-deleted strains, these polymerases do not appear to be the major source of meiotic mutagenicity. From the connection between meiotic mutagenicity and recombination, one may conclude that meiotic recombination has another diversification role, of introducing new mutations at the DNA sequence level, in addition to reshuffling of existing variation. The new, rare meiotic mutations may contribute to long-range evolutionary processes and enhance adaptation to challenging environments.

Indexed as

DNA Breaks, Double-StrandedMeiosisMutationRecombination, GeneticChromosomes, FungalDNA RepairSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiae ProteinsDNA double-strand breaks (DSBs)Homologous recombinationMeiosisMutagenicityMutations

Identifiers

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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.