Evidence map›Paper›PMID 29945904›Full record

ArticleThe Journal of cell biology2018

Actin polymerization controls cilia-mediated signaling.

Michael L Drummond, Mischa Li, Eric Tarapore, Tuyen T L Nguyen, Baina J Barouni, Shaun Cruz, Kevin C Tan, Anthony E Oro, Scott X Atwood

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 88 citations in OpenAlex.

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  15. Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023
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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

9 authors at 2 institutions in 1 country.

Michael L DrummondDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.
Mischa LiDepartment of Dermatology, Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA.ORCID 0000-0001-5452-4529
Eric TaraporeDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.
Tuyen T L NguyenDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.
Baina J BarouniDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.
Shaun CruzDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.
Kevin C TanDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA.ORCID 0000-0002-1729-1444
Anthony E OroDepartment of Dermatology, Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA oro@stanford.edu.
Scott X AtwoodDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, CA satwood@uci.edu.ORCID 0000-0001-7407-9792
University of California, Irvine · USStanford University · US

Funding

BEG4/MIM FUNCTION IN EPITHELIAL NEOPLASIAR01AR052785 · NIAMS · STANFORD UNIVERSITY · PI ORO, ANTHONY E · 2007 to 2018
$4.0M
aPKC function in Hedgehog signaling and basal cell carcinomaR00CA176847 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI ATWOOD, SCOTT · 2015 to 2017
$623k
NCI NIH HHS R00 CA176847NIAMS NIH HHS R01 AR052785
6 · The paper itself

Abstract

Primary cilia are polarized organelles that allow detection of extracellular signals such as Hedgehog (Hh). How the cytoskeleton supporting the cilium generates and maintains a structure that finely tunes cellular response remains unclear. Here, we find that regulation of actin polymerization controls primary cilia and Hh signaling. Disrupting actin polymerization, or knockdown of N-WASp/Arp3, increases ciliation frequency, axoneme length, and Hh signaling. Cdc42, a potent actin regulator, recruits both atypical protein pinase C iota/lambda (aPKC) and Missing-in-Metastasis (MIM) to the basal body to maintain actin polymerization and restrict axoneme length. Transcriptome analysis implicates the Src pathway as a major aPKC effector. aPKC promotes whereas MIM antagonizes Src activity to maintain proper levels of primary cilia, actin polymerization, and Hh signaling. Hh pathway activation requires Smoothened-, Gli-, and Gli1-specific activation by aPKC. Surprisingly, longer axonemes can amplify Hh signaling, except when aPKC is disrupted, reinforcing the importance of the Cdc42-aPKC-Gli axis in actin-dependent regulation of primary cilia signaling.

Indexed as

3T3 CellsActin-Related Protein 3ActinsAnimalsAxonemeBasal Bodiescdc42 GTP-Binding ProteinCell LineCiliaEnzyme ActivationGene Expression RegulationHedgehog ProteinsMiceMicrofilament ProteinsNeoplasm ProteinsPolymerizationActin-Related Protein 3ActinsActr3 protein, mousecdc42 GTP-Binding ProteinCdc42 protein, mouseGli1 protein, mouseHedgehog ProteinsMicrofilament ProteinsMtss1 protein, mouseNeoplasm ProteinsPKC-3 proteinProtein Kinase Csrc-Family KinasesWasl protein, mouseWiskott-Aldrich Syndrome Protein, NeuronalZinc Finger Protein GLI1

Identifiers

PMID29945904
PMCPMC6122990
OpenAlexW2809813982

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.