Evidence map›Paper›PMID 25568333›Full record

ArticleMolecular biology of the cell2015

A mechanism of leading-edge protrusion in the absence of Arp2/3 complex.

Praveen Suraneni, Ben Fogelson, Boris Rubinstein, Philippe Noguera, Niels Volkmann, Dorit Hanein, Alex Mogilner, Rong Li

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. Article
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  3. Article
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Regulation of the Migration of Distinct Dendritic Cell Subsets.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Actin dynamics in cell migration.Essays in biochemistry · 2019
    Review
  17. Review
  18. Article
  19. 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

8 authors.

Praveen SuraneniStowers Institute for Medical Research, Kansas City, MO 64110.
Ben FogelsonCourant Institute and Department of Biology, New York University, New York, NY 10012.
Boris RubinsteinStowers Institute for Medical Research, Kansas City, MO 64110.
Philippe NogueraStowers Institute for Medical Research, Kansas City, MO 64110.
Niels VolkmannBioinformatics and Systems Biology Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037.
Dorit HaneinBioinformatics and Systems Biology Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037.
Alex MogilnerCourant Institute and Department of Biology, New York University, New York, NY 10012.
Rong LiStowers Institute for Medical Research, Kansas City, MO 64110 Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160.

Funding

Structure and function of Arp 2/3 complex--Subproject 4P01GM066311 · NIGMS · YALE UNIVERSITY · PI LI, RONG · 2003 to 2013
$16.8M
Modeling mitotic spindle assemblyR01GM068952 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI MOGILNER, ALEXANDER · 2003 to 2014
$4.4M
NIGMS NIH HHS P01 GM066311NIGMS NIH HHS P01GM 066311NIGMS NIH HHS R01 GM 068952NIGMS NIH HHS R01 GM068952
6 · The paper itself

Abstract

Cells employ protrusive leading edges to navigate and promote their migration in diverse physiological environments. Classical models of leading-edge protrusion rely on a treadmilling dendritic actin network that undergoes continuous assembly nucleated by the Arp2/3 complex, forming ruffling lamellipodia. Recent work demonstrated, however, that, in the absence of the Arp2/3 complex, fibroblast cells adopt a leading edge with filopodia-like protrusions (FLPs) and maintain an ability to move, albeit with altered responses to different environmental signals. We show that formin-family actin nucleators are required for the extension of FLPs but are insufficient to produce a continuous leading edge in fibroblasts lacking Arp2/3 complex. Myosin II is concentrated in arc-like regions of the leading edge in between FLPs, and its activity is required for coordinated advancement of these regions with formin-generated FLPs. We propose that actomyosin contraction acting against membrane tension advances the web of arcs between FLPs. Predictions of this model are verified experimentally. The dependence of myosin II in leading-edge advancement helps explain the previously reported defect in directional movement in the Arpc3-null fibroblasts. We provide further evidence that this defect is cell autonomous during chemotaxis.

Indexed as

ChemotaxisActin CytoskeletonActin-Related Protein 2-3 ComplexActomyosinAnimalsCarrier ProteinsFibroblastsForminsMiceMice, KnockoutMicrotubule-Associated ProteinsMyosin Type IINADPH DehydrogenasePseudopodiaActin-Related Protein 2-3 ComplexActomyosinArpc3 protein, mouseCarrier ProteinsDia2 protein, mouseDiap1 protein, mouseForminsMicrotubule-Associated ProteinsMyosin Type IINADPH Dehydrogenase

Identifiers

PMID25568333
PMCPMC4342026

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LicenceCC BY-NC-SA
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Registered trials

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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.