Evidence map›Paper›PMID 32843356›Full record

ArticleGenetics2020

A dCas9-Based System Identifies a Central Role for Ctf19 in Kinetochore-Derived Suppression of Meiotic Recombination.

Lisa-Marie Kuhl, Vasso Makrantoni, Sarah Recknagel, Animish N Vaze, Adele L Marston, Gerben Vader

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

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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 at 2 institutions in 2 countries.

Lisa-Marie KuhlDepartment of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund 44227, Germany.
Vasso MakrantoniThe Wellcome Centre for Cell Biology, Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, EH9 3BF, United Kingdom.ORCID 0000-0003-0668-6157
Sarah RecknagelDepartment of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund 44227, Germany.
Animish N VazeDepartment of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund 44227, Germany.
Adele L MarstonThe Wellcome Centre for Cell Biology, Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, EH9 3BF, United Kingdom.ORCID 0000-0002-3596-9407
Gerben VaderDepartment of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund 44227, Germany gerben.vader@mpi-dortmund.mpg.de.ORCID 0000-0001-5729-0991
Max Planck Institute of Molecular Physiology · DEWellcome Centre for Cell Biology · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

In meiosis, crossover (CO) formation between homologous chromosomes is essential for faithful segregation. However, misplaced meiotic recombination can have catastrophic consequences on genome stability. Within pericentromeres, COs are associated with meiotic chromosome missegregation. In organisms ranging from yeast to humans, pericentromeric COs are repressed. We previously identified a role for the kinetochore-associated Ctf19 complex (Ctf19c) in pericentromeric CO suppression. Here, we develop a dCas9/CRISPR-based system that allows ectopic targeting of Ctf19c-subunits. Using this approach, we query sufficiency in meiotic CO suppression, and identify Ctf19 as a mediator of kinetochore-associated CO control. The effect of Ctf19 is encoded in its NH2-terminal tail, and depends on residues important for the recruitment of the Scc2-Scc4 cohesin regulator. This work provides insight into kinetochore-derived control of meiotic recombination. We establish an experimental platform to investigate and manipulate meiotic CO control. This platform can easily be adapted in order to investigate other aspects of chromosome biology.

Indexed as

Crossing Over, GeneticSuppression, GeneticChromosomal Proteins, Non-HistoneCytoskeletal ProteinsKinetochoresMeiosisProtein DomainsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsChromosomal Proteins, Non-HistoneCTF19 protein, S cerevisiaeCytoskeletal ProteinsSaccharomyces cerevisiae ProteinsSCC2 protein, S cerevisiaeSCC4 protein, S cerevisiaeCRISPRdCas9kinetochoremeiosisrecombination

Identifiers

PMID32843356
PMCPMC7536843
OpenAlexW3081290228

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.