Evidence map›Paper›PMID 26755742›Full record

ArticleEMBO reports2016

A non-canonical function of Plk4 in centriolar satellite integrity and ciliogenesis through PCM1 phosphorylation.

Akiko Hori, Karin Barnouin, Ambrosius P Snijders, Takashi Toda

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

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  6. Post-Translational Modifications in Cilia and Ciliopathies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
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  9. Permanent cilia loss during cerebellar granule cell neurogenesis involves withdrawal of cilia maintenance and centriole capping.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
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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

4 authors at 2 institutions in 2 countries.

Akiko HoriThe Francis Crick Institute, Lincoln's Inn Fields Laboratory, London, UK Developmental Biomedical Science, Graduate School of Biological Sciences, Nara Institute of Science and Technology (NAIST), Ikoma Nara, Japan.
Karin BarnouinThe Francis Crick Institute, Clare Hall Laboratory, London, UK.
Ambrosius P SnijdersThe Francis Crick Institute, Clare Hall Laboratory, London, UK.
Takashi TodaThe Francis Crick Institute, Lincoln's Inn Fields Laboratory, London, UK Hiroshima Research Center for Healthy Aging (HiHA), Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter Hiroshima University, Higashi-Hiroshima, Japan takashi-toda@hiroshima-u.ac.jp.
The Francis Crick Institute · GBNara Institute of Science and Technology · JP

Funding

Cancer Research UK
6 · The paper itself

Abstract

Centrioles are the major constituents of the animal centrosome, in which Plk4 kinase serves as a master regulator of the duplication cycle. Many eukaryotes also contain numerous peripheral particles known as centriolar satellites. While centriolar satellites aid centriole assembly and primary cilium formation, it is unknown whether Plk4 plays any regulatory roles in centriolar satellite integrity. Here we show that Plk4 is a critical determinant of centriolar satellite organisation. Plk4 depletion leads to the dispersion of centriolar satellites and perturbed ciliogenesis. Plk4 interacts with the satellite component PCM1, and its kinase activity is required for phosphorylation of the conserved S372. The nonphosphorylatable PCM1 mutant recapitulates phenotypes of Plk4 depletion, while the phosphomimetic mutant partially rescues the dispersed centriolar satellite patterns and ciliogenesis in cells depleted of PCM1. We show that S372 phosphorylation occurs during the G1 phase of the cell cycle and is important for PCM1 dimerisation and interaction with other satellite components. Our findings reveal that Plk4 is required for centriolar satellite function, which may underlie the ciliogenesis defects caused by Plk4 dysfunction.

Indexed as

Protein Processing, Post-TranslationalAutoantigensCell Cycle ProteinsCentriolesCiliaG1 PhaseHeLa CellsHumansPhosphorylationProtein BindingProtein MultimerizationProtein Serine-Threonine KinasesAutoantigensCell Cycle ProteinsPCM1 protein, humanPLK4 protein, humanProtein Serine-Threonine Kinasescentriolar satellitescentrosomeciliogenesisPCM1Plk4

Identifiers

PMID26755742
PMCPMC4772974
OpenAlexW2289819671

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.