Evidence map›Paper›PMID 35876814›Full record

ArticleGenetics2022

Turning coldspots into hotspots: targeted recruitment of axis protein Hop1 stimulates meiotic recombination in Saccharomyces cerevisiae.

Anura Shodhan, Martin Xaver, David Wheeler, Michael Lichten

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Absence of chromosome axis protein recruitment prevents meiotic recombination chromosome-wide in the budding yeastProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. 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

4 authors at 1 institution in 1 country.

Anura ShodhanLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.ORCID 0000-0002-3675-2146
Martin XaverLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.ORCID 0000-0002-0722-466X
David WheelerLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.ORCID 0000-0002-2929-4204
Michael LichtenLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.ORCID 0000-0001-9707-2956
National Cancer Institute · US

Funding

Mechanism of Meiotic RecombinationZIABC005268 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LICHTEN, MICHAEL J · 2009 to 2023
$17.3M
6 · The paper itself

Abstract

The DNA double-strand breaks that initiate meiotic recombination are formed in the context of the meiotic chromosome axis, which in Saccharomyces cerevisiae contains a meiosis-specific cohesin isoform and the meiosis-specific proteins Hop1 and Red1. Hop1 and Red1 are important for double-strand break formation; double-strand break levels are reduced in their absence and their levels, which vary along the lengths of chromosomes, are positively correlated with double-strand break levels. How axis protein levels influence double-strand break formation and recombination remains unclear. To address this question, we developed a novel approach that uses a bacterial ParB-parS partition system to recruit axis proteins at high levels to inserts at recombination coldspots where Hop1 and Red1 levels are normally low. Recruiting Hop1 markedly increased double-strand breaks and homologous recombination at target loci, to levels equivalent to those observed at endogenous recombination hotspots. This local increase in double-strand breaks did not require Red1 or the meiosis-specific cohesin component Rec8, indicating that, of the axis proteins, Hop1 is sufficient to promote double-strand break formation. However, while most crossovers at endogenous recombination hotspots are formed by the meiosis-specific MutLγ resolvase, crossovers that formed at an insert locus were only modestly reduced in the absence of MutLγ, regardless of whether or not Hop1 was recruited to that locus. Thus, while local Hop1 levels determine local double-strand break levels, the recombination pathways that repair these breaks can be determined by other factors, raising the intriguing possibility that different recombination pathways operate in different parts of the genome.

Indexed as

Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDNA Breaks, Double-StrandedHomologous RecombinationMeiosisChromosomal Proteins, Non-HistoneDNA-Binding ProteinsHOP1 protein, S cerevisiaeREC8 protein, S cerevisiaeSaccharomyces cerevisiae Proteinschromosome axiscrossing overdouble-strand breaksHop1meiosismeiotic recombinationrecombination pathways

Identifiers

PMID35876814
PMCPMC9434160
OpenAlexW4287447640

What OpenQuestion holds

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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.