Evidence map›Paper›PMID 27112294›Full record

ArticleCurrent biology : CB2016

Tropomyosin Promotes Lamellipodial Persistence by Collaborating with Arp2/3 at the Leading Edge.

Simon Brayford, Nicole S Bryce, Galina Schevzov, Elizabeth M Haynes, James E Bear, Edna C Hardeman, Peter W Gunning

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-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

33 citing papers in PubMed, 48 citations in OpenAlex.

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  20. Actin-tropomyosin distribution in non-muscle cells.Journal of muscle research and cell motility · 2020
    Review
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

7 authors at 2 institutions in 2 countries.

Simon BrayfordOncology Research Unit, School of Medical Sciences, UNSW Australia, Sydney, NSW 2052, Australia.
Nicole S BryceOncology Research Unit, School of Medical Sciences, UNSW Australia, Sydney, NSW 2052, Australia.
Galina SchevzovOncology Research Unit, School of Medical Sciences, UNSW Australia, Sydney, NSW 2052, Australia.
Elizabeth M HaynesDepartment of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599-3280, USA.
James E BearDepartment of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599-3280, USA.
Edna C HardemanCellular and Genetic Medicine Unit, School of Medical Sciences, UNSW Australia, Sydney, NSW 2052, Australia.
Peter W GunningOncology Research Unit, School of Medical Sciences, UNSW Australia, Sydney, NSW 2052, Australia. Electronic address: p.gunning@unsw.edu.au.
UNSW Sydney · AUUniversity of North Carolina at Chapel Hill · US

Funding

The role of the Arp2/3 complex in cellular actin dynamicsR01GM111557 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BEAR, JAMES E · 2014 to 2018
$1.5M
NIGMS NIH HHS R01 GM111557
6 · The paper itself

Abstract

At the leading edge of migrating cells, protrusion of the lamellipodium is driven by Arp2/3-mediated polymerization of actin filaments [1]. This dense, branched actin network is promoted and stabilized by cortactin [2, 3]. In order to drive filament turnover, Arp2/3 networks are remodeled by proteins such as GMF, which blocks the actin-Arp2/3 interaction [4, 5], and coronin 1B, which acts by directing SSH1L to the lamellipodium where it activates the actin-severing protein cofilin [6, 7]. It has been shown in vitro that cofilin-mediated severing of Arp2/3 actin networks results in the generation of new pointed ends to which the actin-stabilizing protein tropomyosin (Tpm) can bind [8]. The presence of Tpm in lamellipodia, however, is disputed in the literature [9-19]. Here, we report that the Tpm isoforms 1.8/9 are enriched in the lamellipodium of fibroblasts as detected with a novel isoform-specific monoclonal antibody. RNAi-mediated silencing of Tpm1.8/9 led to an increase of Arp2/3 accumulation at the cell periphery and a decrease in the persistence of lamellipodia and cell motility, a phenotype consistent with cortactin- and coronin 1B-deficient cells [2, 7]. In the absence of coronin 1B or cofilin, Tpm1.8/9 protein levels are reduced while, conversely, inhibition of Arp2/3 with CK666 leads to an increase in Tpm1.8/9 protein. These findings establish a novel regulatory mechanism within the lamellipodium whereby Tpm collaborates with Arp2/3 to promote lamellipodial-based cell migration.

Indexed as

Actin CytoskeletonActin-Related Protein 2-3 ComplexFibroblastsHumansPolymerizationProtein IsoformsPseudopodiaTropomyosinActin-Related Protein 2-3 ComplexProtein IsoformsTPM1 protein, humanTropomyosin

Identifiers

PMID27112294
PMCPMC5644994
OpenAlexW2338269936

What OpenQuestion holds

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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.