Evidence map›Paper›PMID 37888778›Full record

ArticleEMBO reports2023

PLK1 promotes the mitotic surveillance pathway by controlling cytosolic 53BP1 availability.

Matteo Burigotto, Vincenza Vigorito, Colin Gliech, Alessia Mattivi, Sabrina Ghetti, Alessandra Bisio, Graziano Lolli, Andrew J Holland, Luca L Fava

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  9. When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  10. 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

9 authors at 4 institutions in 3 countries.

Matteo Burigotto *Armenise-Harvard Laboratory of Cell Division, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.ORCID 0000-0003-1891-4057
Vincenza Vigorito *Armenise-Harvard Laboratory of Cell Division, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.
Colin GliechDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-5410-1718
Alessia MattiviArmenise-Harvard Laboratory of Cell Division, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.
Sabrina GhettiArmenise-Harvard Laboratory of Cell Division, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.ORCID 0000-0002-4981-9012
Alessandra BisioLaboratory of Radiobiology, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.ORCID 0000-0002-3326-1923
Graziano LolliLaboratory of Protein Crystallography and Structure-Based Drug Design, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.ORCID 0000-0002-8536-5599
Andrew J HollandOncology Research, Amgen Research, Thousand Oaks, CA, USA.
Luca L FavaArmenise-Harvard Laboratory of Cell Division, Department of Cellular, Computational and Integrative Biology - CIBIO, University of Trento, Trento, Italy.ORCID 0000-0002-6741-1723
University of Trento · ITAmgen (United States) · USJohns Hopkins University · USKing's College London · GB

Funding

Centrosome biogenesis and copy number controlR01GM114119 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI CORMACK, BRENDAN · 2015 to 2023
$3.3M
EC | European Regional Development Fund (ERDF)Fondazione AIRC per la ricerca sul cancro ETS (AIRC) 23560Fondazione Telethon (FT) GJC21181Giovanni Armenise-Harvard Foundation (GAHF) CDA 2017Ministero dell'Università e della Ricerca (MUR) CUP E64I19001070001NIGMS NIH HHS R01 GM114119
6 · The paper itself

Abstract

53BP1 acts at the crossroads between DNA repair and p53-mediated stress response. With its interactors p53 and USP28, it is part of the mitotic surveillance (or mitotic stopwatch) pathway (MSP), a sensor that monitors the duration of cell division, promoting p53-dependent cell cycle arrest when a critical time threshold is surpassed. Here, we show that Polo-like kinase 1 (PLK1) activity is essential for the time-dependent release of 53BP1 from kinetochores. PLK1 inhibition, which leads to 53BP1 persistence at kinetochores, prevents cytosolic 53BP1 association with p53 and results in a blunted MSP. Strikingly, the identification of CENP-F as the kinetochore docking partner of 53BP1 enabled us to show that measurement of mitotic timing by the MSP does not take place at kinetochores, as perturbing CENP-F-53BP1 binding had no measurable impact on the MSP. Taken together, we propose that PLK1 supports the MSP by generating a cytosolic pool of 53BP1 and that an unknown cytosolic mechanism enables the measurement of mitotic duration.

Indexed as

Cell Cycle ProteinsProtein Serine-Threonine KinasesHeLa CellsHumansKinetochoresMitosisPolo-Like Kinase 1Tumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53Ubiquitin ThiolesteraseCell Cycle ProteinsPLK1 protein, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53Ubiquitin ThiolesteraseUSP28 protein, human53BP1kinetochoremitotic stopwatch pathwaymitotic surveillance pathwayPLK1

Identifiers

PMID37888778
PMCPMC10702821
OpenAlexW4387965882

What OpenQuestion holds

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LicenceCC BY
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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.