Evidence map›Paper›PMID 28100636›Full record

ArticleMolecular biology of the cell2017

Centriole splitting caused by loss of the centrosomal linker protein C-NAP1 reduces centriolar satellite density and impedes centrosome amplification.

Anne-Marie Flanagan, Elena Stavenschi, Shivakumar Basavaraju, David Gaboriau, David A Hoey, Ciaran G Morrison

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Roles for ELMOD2 and Rootletin in ciliogenesis.Molecular biology of the cell · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. A homozygous founder missense variant in arylsulfatase G abolishes its enzymatic activity causing atypical Usher syndrome in humans.Genetics in medicine : official journal of the American College of Medical Genetics · 2018
    Article
  18. Article
  19. Building the right centriole for each cell type.The Journal of cell biology · 2018
    Review
  20. Article
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

6 authors at 3 institutions in 1 country.

Anne-Marie FlanaganCentre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland.
Elena StavenschiTrinity Centre for Bioengineering, Trinity Biomedical Sciences Institute, and.
Shivakumar BasavarajuCentre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland.
David GaboriauCentre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland.
David A HoeyTrinity Centre for Bioengineering, Trinity Biomedical Sciences Institute, and.
Ciaran G MorrisonCentre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland Ciaran.Morrison@nuigalway.ie.
Ollscoil na Gaillimhe – University of Galway · IERoyal College of Surgeons in Ireland · IETrinity College Dublin · IE

Funding

European Research Council 336882
6 · The paper itself

Abstract

Duplication of the centrosomes is a tightly regulated process. Abnormal centrosome numbers can impair cell division and cause changes in how cells migrate. Duplicated centrosomes are held together by a proteinaceous linker made up of rootletin filaments anchored to the centrioles by C-NAP1. This linker is removed in a NEK2A kinase-dependent manner as mitosis begins. To explore C-NAP1 activities in regulating centrosome activities, we used genome editing to ablate it. C-NAP1-null cells were viable and had an increased frequency of premature centriole separation, accompanied by reduced density of the centriolar satellites, with reexpression of C-NAP1 rescuing both phenotypes. We found that the primary cilium, a signaling structure that arises from the mother centriole docked to the cell membrane, was intact in the absence of C-NAP1, although components of the ciliary rootlet were aberrantly localized away from the base of the cilium. C-NAP1-deficient cells were capable of signaling through the cilium, as determined by gene expression analysis after fluid flow-induced shear stress and the relocalization of components of the Hedgehog pathway. Centrosome amplification induced by DNA damage or by PLK4 or CDK2 overexpression was markedly reduced in the absence of C-NAP1. We conclude that centriole splitting reduces the local density of key centriolar precursors to impede overduplication.

Indexed as

AutoantigensCell CycleCell Cycle ProteinsCell LineCentriolesCentrosomeCiliaHumansMitosisSignal TransductionSpindle ApparatusAutoantigensCell Cycle ProteinsCEP250 protein, human

Identifiers

PMID28100636
PMCPMC5349781
OpenAlexW2579376414

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.