Evidence map›Paper›PMID 28694245›Full record

ArticleThe EMBO journal2017

Fundamental cell cycle kinases collaborate to ensure timely destruction of the synaptonemal complex during meiosis.

Bilge Argunhan, Wing-Kit Leung, Negar Afshar, Yaroslav Terentyev, Vijayalakshmi V Subramanian, Yasuto Murayama, Andreas Hochwagen, Hiroshi Iwasaki, Tomomi Tsubouchi, Hideo Tsubouchi

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

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  3. bioRxiv : the preprint server for biology · 2026
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  11. Polycomb group (PcG) proteins prevent the assembly of abnormal synaptonemal complex structures during meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Bilge ArgunhanGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK.ORCID 0000-0002-6023-7654
Wing-Kit LeungGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK.
Negar AfsharGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK.
Yaroslav TerentyevGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK.
Vijayalakshmi V SubramanianDepartment of Biology, New York University, New York, NY, USA.ORCID 0000-0003-4037-3832
Yasuto MurayamaInstitute of Innovative Research, Tokyo Institute of Technology, Tokyo, Japan.
Andreas HochwagenDepartment of Biology, New York University, New York, NY, USA.
Hiroshi IwasakiInstitute of Innovative Research, Tokyo Institute of Technology, Tokyo, Japan.
Tomomi TsubouchiGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK ttsubo@nibb.ac.jp htsubo@nibb.ac.jp.
Hideo TsubouchiGenome Damage and Stability Centre, Life Sciences, University of Sussex, Brighton, East Sussex, UK ttsubo@nibb.ac.jp htsubo@nibb.ac.jp.ORCID 0000-0003-0814-8432
Tokyo Institute of Technology · JPNational Institute for Basic Biology · JPNew York University · USUniversity of Sussex · GB

Funding

Mechanisms of Chromosome Scale Signal PropagationR01GM111715 · NIGMS · NEW YORK UNIVERSITY · PI HOCHWAGEN, ANDREAS · 2015 to 2022
$2.6M
Biotechnology and Biological Sciences Research Council BB/I009159/1NIGMS NIH HHS R01 GM111715
6 · The paper itself

Abstract

The synaptonemal complex (SC) is a proteinaceous macromolecular assembly that forms during meiotic prophase I and mediates adhesion of paired homologous chromosomes along their entire lengths. Although prompt disassembly of the SC during exit from prophase I is a landmark event of meiosis, the underlying mechanism regulating SC destruction has remained elusive. Here, we show that DDK (Dbf4-dependent Cdc7 kinase) is central to SC destruction. Upon exit from prophase I, Dbf4, the regulatory subunit of DDK, directly associates with and is phosphorylated by the Polo-like kinase Cdc5. In parallel, upregulated CDK1 activity also targets Dbf4. An enhanced Dbf4-Cdc5 interaction pronounced phosphorylation of Dbf4 and accelerated SC destruction, while reduced/abolished Dbf4 phosphorylation hampered destruction of SC proteins. SC destruction relieved meiotic inhibition of the ubiquitous recombinase Rad51, suggesting that the mitotic recombination machinery is reactivated following prophase I exit to repair any persisting meiotic DNA double-strand breaks. Taken together, we propose that the concerted action of DDK, Polo-like kinase, and CDK1 promotes efficient SC destruction at the end of prophase I to ensure faithful inheritance of the genome.

Indexed as

Cell Cycle ProteinsFungal ProteinsMeiosisPhosphorylationProtein KinasesSaccharomycetalesSynaptonemal ComplexCell Cycle ProteinsFungal ProteinsProtein KinasesDbf4‐dependent Cdc7 kinasehomologous recombinationmeiosisPolo‐like kinasesynaptonemal complex

Identifiers

PMID28694245
PMCPMC5579384
OpenAlexW2735911592

What OpenQuestion holds

Textmetadata
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.