Evidence map›Paper›PMID 25658810›Full record

ArticlePloS one2015

Multiple requirements of PLK1 during mouse oocyte maturation.

Petr Solc, Tomoya S Kitajima, Shuhei Yoshida, Adela Brzakova, Masako Kaido, Vladimir Baran, Alexandra Mayer, Pavlina Samalova, Jan Motlik, Jan Ellenberg

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 101 citations in OpenAlex.

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  9. Polo-like kinase 1 prevents excess microtubule polymerization inbioRxiv : the preprint server for biology · 2024
    Article
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  12. The signal that stimulates mammalian embryo development.Frontiers in cell and developmental biology · 2024
    Review
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  15. Article
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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

10 authors at 3 institutions in 3 countries.

Petr SolcInstitute of Animal Physiology and Genetics, Libechov, Czech Republic.
Tomoya S KitajimaCell Biology and Biophysics Unit, European Molecular Biology Laboratory, Heidelberg, Germany; Laboratory for Chromosome Segregation, RIKEN Center for Developmental Biology, Kobe, Japan.
Shuhei YoshidaLaboratory for Chromosome Segregation, RIKEN Center for Developmental Biology, Kobe, Japan.
Adela BrzakovaInstitute of Animal Physiology and Genetics, Libechov, Czech Republic.
Masako KaidoLaboratory for Chromosome Segregation, RIKEN Center for Developmental Biology, Kobe, Japan.
Vladimir BaranInstitute of Animal Physiology, Kosice, Slovakia.
Alexandra MayerInstitute of Animal Physiology and Genetics, Libechov, Czech Republic.
Pavlina SamalovaInstitute of Animal Physiology and Genetics, Libechov, Czech Republic.
Jan MotlikInstitute of Animal Physiology and Genetics, Libechov, Czech Republic.
Jan EllenbergCell Biology and Biophysics Unit, European Molecular Biology Laboratory, Heidelberg, Germany.
Czech Academy of Sciences, Institute of Animal Physiology and Genetics · CZEuropean Molecular Biology Laboratory · DEInstitute of Animal Physiology of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polo-like kinase 1 (PLK1) orchestrates multiple events of cell division. Although PLK1 function has been intensively studied in centriole-containing and rapidly cycling somatic cells, much less is known about its function in the meiotic divisions of mammalian oocytes, which arrest for a long period of time in prophase before meiotic resumption and lack centrioles for spindle assembly. Here, using specific small molecule inhibition combined with live mouse oocyte imaging, we comprehensively characterize meiotic PLK1's functions. We show that PLK1 becomes activated at meiotic resumption on microtubule organizing centers (MTOCs) and later at kinetochores. PLK1 is required for efficient meiotic resumption by promoting nuclear envelope breakdown. PLK1 is also needed to recruit centrosomal proteins to acentriolar MTOCs to promote normal spindle formation, as well as for stable kinetochore-microtubule attachment. Consequently, PLK1 inhibition leads to metaphase I arrest with misaligned chromosomes activating the spindle assembly checkpoint (SAC). Unlike in mitosis, the metaphase I arrest is not bypassed by the inactivation of the SAC. We show that PLK1 is required for the full activation of the anaphase promoting complex/cyclosome (APC/C) by promoting the degradation of the APC/C inhibitor EMI1 and is therefore essential for entry into anaphase I. Moreover, our data suggest that PLK1 is required for proper chromosome segregation and the maintenance of chromosome condensation during the meiosis I-II transition, independently of the APC/C. Thus, our results define the meiotic roles of PLK1 in oocytes and reveal interesting differential requirements of PLK1 between mitosis and oocyte meiosis in mammals.

Indexed as

Anaphase-Promoting Complex-CyclosomeAnimalsBlotting, WesternCell Cycle ProteinsChromosome SegregationFemaleImage Processing, Computer-AssistedKinetochoresMeiosisMiceMicroscopy, ConfocalMicrotubule-Organizing CenterNuclear EnvelopeOocytesPolo-Like Kinase 1Protein Serine-Threonine KinasesAnaphase-Promoting Complex-CyclosomeCell Cycle ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene Proteins

Identifiers

PMID25658810
PMCPMC4319955
OpenAlexW1974854171

What OpenQuestion holds

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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.