Evidence map›Paper›PMID 26150389›Full record

ArticleThe Journal of cell biology2015

p53 protects against genome instability following centriole duplication failure.

Bramwell G Lambrus, Yumi Uetake, Kevin M Clutario, Vikas Daggubati, Michael Snyder, Greenfield Sluder, Andrew J Holland

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 150 citations in OpenAlex.

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  20. Regulation of adult stem cell function by ketone bodies.Frontiers in cell and developmental biology · 2023
    Review

36 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Bramwell G LambrusDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Yumi UetakeDepartment of Cell and Developmental Biology, University of Massachusetts Medical School, Worcester, MA 01655.
Kevin M ClutarioDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Vikas DaggubatiDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Michael SnyderDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Greenfield SluderDepartment of Cell and Developmental Biology, University of Massachusetts Medical School, Worcester, MA 01655.
Andrew J HollandDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205 aholland@jhmi.edu.
Johns Hopkins Medicine · USUniversity of Massachusetts Chan Medical School · USJohns Hopkins University · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
RNA IN FORMATION, FUNCTION, AND REPRODUCTION OF CENTROSOR01GM030758 · NIGMS · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI SLUDER, GREENFIELD · 1985 to 2014
$6.4M
Centrosome biogenesis and copy number controlR01GM114119 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI CORMACK, BRENDAN · 2015 to 2023
$3.3M
NIGMS NIH HHS GM 114119NIGMS NIH HHS GM30758NIGMS NIH HHS R01 GM030758NIGMS NIH HHS R01 GM114119NIGMS NIH HHS T32 GM007445
6 · The paper itself

Abstract

Centriole function has been difficult to study because of a lack of specific tools that allow persistent and reversible centriole depletion. Here we combined gene targeting with an auxin-inducible degradation system to achieve rapid, titratable, and reversible control of Polo-like kinase 4 (Plk4), a master regulator of centriole biogenesis. Depletion of Plk4 led to a failure of centriole duplication that produced an irreversible cell cycle arrest within a few divisions. This arrest was not a result of a prolonged mitosis, chromosome segregation errors, or cytokinesis failure. Depleting p53 allowed cells that fail centriole duplication to proliferate indefinitely. Washout of auxin and restoration of endogenous Plk4 levels in cells that lack centrioles led to the penetrant formation of de novo centrioles that gained the ability to organize microtubules and duplicate. In summary, we uncover a p53-dependent surveillance mechanism that protects against genome instability by preventing cell growth after centriole duplication failure.

Indexed as

Genomic InstabilityCell Cycle CheckpointsCell LineCell ProliferationCentriolesChromosome SegregationHumansMicrotubulesMitosisProtein Serine-Threonine KinasesProtein TransportTumor Suppressor Protein p53PLK4 protein, humanProtein Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26150389
PMCPMC4494000
OpenAlexW1922047550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.