Evidence map›Paper›PMID 25996914›Full record

ArticlePLoS genetics2015

Clustering and negative feedback by endocytosis in planar cell polarity signaling is modulated by ubiquitinylation of prickle.

Bomsoo Cho, Gandhy Pierre-Louis, Andreas Sagner, Suzanne Eaton, Jeffrey D Axelrod

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Deubiquitination of Vangl by USP6 and USP32 Regulates Planar Cell Polarity Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

5 authors at 2 institutions in 2 countries.

Bomsoo ChoDepartment of Pathology, Stanford University School of Medicine, Stanford, California, United States of America.
Gandhy Pierre-LouisDepartment of Pathology, Stanford University School of Medicine, Stanford, California, United States of America; Department of Developmental Biology, Stanford University School of Medicine, Stanford, California, United States of America.
Andreas SagnerMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Suzanne EatonMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Jeffrey D AxelrodDepartment of Pathology, Stanford University School of Medicine, Stanford, California, United States of America.
Stanford University · USMax Planck Institute of Molecular Cell Biology and Genetics · DE

Funding

GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
TRAINING & OUTREACH COREP50GM107615 · NIGMS · STANFORD UNIVERSITY · PI COVERT, MARKUS W · 2013 to 2017
$10.9M
Signaling mechanisms Controlling Planar Cell PolarityR37GM059823 · NIGMS · STANFORD UNIVERSITY · PI AXELROD, JEFFREY D. · 2014 to 2018
$1.8M
NIGMS NIH HHS 5T32GM007790NIGMS NIH HHS P50 GM107615NIGMS NIH HHS R37 GM059823NIGMS NIH HHS T32 GM007790
6 · The paper itself

Abstract

The core components of the planar cell polarity (PCP) signaling system, including both transmembrane and peripheral membrane associated proteins, form asymmetric complexes that bridge apical intercellular junctions. While these can assemble in either orientation, coordinated cell polarization requires the enrichment of complexes of a given orientation at specific junctions. This might occur by both positive and negative feedback between oppositely oriented complexes, and requires the peripheral membrane associated PCP components. However, the molecular mechanisms underlying feedback are not understood. We find that the E3 ubiquitin ligase complex Cullin1(Cul1)/SkpA/Supernumerary limbs(Slimb) regulates the stability of one of the peripheral membrane components, Prickle (Pk). Excess Pk disrupts PCP feedback and prevents asymmetry. We show that Pk participates in negative feedback by mediating internalization of PCP complexes containing the transmembrane components Van Gogh (Vang) and Flamingo (Fmi), and that internalization is activated by oppositely oriented complexes within clusters. Pk also participates in positive feedback through an unknown mechanism promoting clustering. Our results therefore identify a molecular mechanism underlying generation of asymmetry in PCP signaling.

Indexed as

Cell PolarityEndocytosisUbiquitinationAnimalsCluster AnalysisCullin ProteinsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEpithelial CellsLIM Domain ProteinsMembrane ProteinsSignal TransductionUbiquitin-Protein LigasesWings, AnimalCullin 1Cullin ProteinsDNA-Binding ProteinsDrosophila ProteinsLIM Domain ProteinsMembrane Proteinspk protein, DrosophilaUbiquitin-Protein Ligases

Identifiers

PMID25996914
PMCPMC4440771
OpenAlexW223028927

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.