Evidence map›Paper›PMID 25688134›Full record

ArticleThe Journal of cell biology2015

Two Polo-like kinase 4 binding domains in Asterless perform distinct roles in regulating kinase stability.

Joseph E Klebba, Brian J Galletta, Jonathan Nye, Karen M Plevock, Daniel W Buster, Natalie A Hollingsworth, Kevin C Slep, Nasser M Rusan, Gregory C Rogers

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Generating CRISPR-edited clonal lines of culturedBiology methods & protocols · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Journal of cell science · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  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

9 authors at 5 institutions in 1 country.

Joseph E KlebbaDepartment of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724.
Brian J GallettaNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Jonathan NyeDepartment of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724.
Karen M PlevockNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.
Daniel W BusterDepartment of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724.
Natalie A HollingsworthDepartment of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724.
Kevin C SlepDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.
Nasser M RusanNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 nasser.rusan@nih.gov gcrogers@email.arizona.edu.
Gregory C RogersDepartment of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, University of Arizona, Tucson, AZ 85724 nasser.rusan@nih.gov gcrogers@email.arizona.edu.
University of Arizona · USUniversity of Arizona Cancer CenterUniversity of North Carolina at Chapel Hill · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Regulating Centrosome Duplication and MaturationZIAHL006104 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI RUSAN, NASSER · 2011 to 2021
$8.6M
Molecular Mechanisms of Cytoskeletal RegulatorsR01GM094415 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROGERS, STEPHEN, SLEP, KEVIN C · 2011 to 2014
$1.1M
Intramural NIH HHS ZIA HL006104NCI NIH HHS 30 CA23074NCI NIH HHS P30 CA023074NIGMS NIH HHS R01 GM094415NIGMS NIH HHS R01GM094415
6 · The paper itself

Abstract

Plk4 (Polo-like kinase 4) and its binding partner Asterless (Asl) are essential, conserved centriole assembly factors that induce centriole amplification when overexpressed. Previous studies found that Asl acts as a scaffolding protein; its N terminus binds Plk4's tandem Polo box cassette (PB1-PB2) and targets Plk4 to centrioles to initiate centriole duplication. However, how Asl overexpression drives centriole amplification is unknown. In this paper, we investigated the Asl-Plk4 interaction in Drosophila melanogaster cells. Surprisingly, the N-terminal region of Asl is not required for centriole duplication, but a previously unidentified Plk4-binding domain in the C terminus is required. Mechanistic analyses of the different Asl regions revealed that they act uniquely during the cell cycle: the Asl N terminus promotes Plk4 homodimerization and autophosphorylation during interphase, whereas the Asl C terminus stabilizes Plk4 during mitosis. Therefore, Asl affects Plk4 in multiple ways to regulate centriole duplication. Asl not only targets Plk4 to centrioles but also modulates Plk4 stability and activity, explaining the ability of overexpressed Asl to drive centriole amplification.

Indexed as

AnimalsCell CycleCell Cycle ProteinsCell LineCentriolesDrosophila melanogasterDrosophila ProteinsEnzyme StabilityMitosisPhosphorylationProtein BindingProtein MultimerizationProtein Serine-Threonine KinasesProtein Structure, TertiaryRNA InterferenceRNA, Small InterferingAsl protein, DrosophilaCell Cycle ProteinsDrosophila ProteinsProtein Serine-Threonine KinasesRNA, Small InterferingSak protein, Drosophila

Identifiers

PMID25688134
PMCPMC4332252
OpenAlexW2065361551

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.