Evidence map›Paper›PMID 27091449›Full record

ArticleThe Journal of cell biology2016

A requirement for filopodia extension toward Slit during Robo-mediated axon repulsion.

Russell E McConnell, J Edward van Veen, Marina Vidaki, Adam V Kwiatkowski, Aaron S Meyer, Frank B Gertler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Russell E McConnellDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 01239.
J Edward van VeenDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 01239 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 01239.
Marina VidakiDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 01239.
Adam V KwiatkowskiDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 01239.
Aaron S MeyerDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 01239 Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 01239.
Frank B GertlerDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 01239 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 01239 fgertler@mit.edu.
Massachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Cytoskeletal Regulation During Growth Cone Migration and Axon GuidanceR01GM068678 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GERTLER, FRANK B · 2003 to 2012
$2.6M
Role of Phospho-Tyrosine Binding in Mena-Driven MetastasisF32CA165700 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MCCONNELL, RUSSELL E. · 2012 to 2014
$156k
NCI NIH HHS F32 CA165700NCI NIH HHS P30 CA014051NIGMS NIH HHS R01 GM068678
6 · The paper itself

Abstract

Axons navigate long distances through complex 3D environments to interconnect the nervous system during development. Although the precise spatiotemporal effects of most axon guidance cues remain poorly characterized, a prevailing model posits that attractive guidance cues stimulate actin polymerization in neuronal growth cones whereas repulsive cues induce actin disassembly. Contrary to this model, we find that the repulsive guidance cue Slit stimulates the formation and elongation of actin-based filopodia from mouse dorsal root ganglion growth cones. Surprisingly, filopodia form and elongate toward sources of Slit, a response that we find is required for subsequent axonal repulsion away from Slit. Mechanistically, Slit evokes changes in filopodium dynamics by increasing direct binding of its receptor, Robo, to members of the actin-regulatory Ena/VASP family. Perturbing filopodium dynamics pharmacologically or genetically disrupts Slit-mediated repulsion and produces severe axon guidance defects in vivo. Thus, Slit locally stimulates directional filopodial extension, a process that is required for subsequent axonal repulsion downstream of the Robo receptor.

Indexed as

AnimalsAxonsChemotaxisEmbryonic DevelopmentGlycoproteinsGrowth ConesHEK293 CellsHumansMiceNerve Tissue ProteinsPseudopodiaReceptors, ImmunologicRoundabout ProteinsSignal TransductionGlycoproteinsNerve Tissue ProteinsReceptors, ImmunologicRoundabout Proteinsslit protein, vertebrate

Identifiers

PMID27091449
PMCPMC5084274
OpenAlexW2338864125

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.