Evidence map›Paper›PMID 26304727›Full record

ArticleThe Journal of cell biology2015

Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair.

Miranda V Hunter, Donghoon M Lee, Tony J C Harris, Rodrigo Fernandez-Gonzalez

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-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

34 citing papers in PubMed, 86 citations in OpenAlex.

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  11. IRF6 Regulates the Delivery of E-Cadherin to the Plasma Membrane.The Journal of investigative dermatology · 2022
    Article
  12. Optochemical Control of Cell Contractility in Drosophila Embryos.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  13. Saudi journal of biological sciences · 2021
    Article
  14. Article
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  17. Review
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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

4 authors at 1 institution in 1 country.

Miranda V HunterDepartment of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Donghoon M LeeDepartment of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Tony J C HarrisDepartment of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Rodrigo Fernandez-GonzalezDepartment of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario M5S 3G9, Canada Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada rodrigo.fernandez.gonzalez@utoronto.ca.
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Embryonic epithelia have a remarkable ability to rapidly repair wounds. A supracellular actomyosin cable around the wound coordinates cellular movements and promotes wound closure. Actomyosin cable formation is accompanied by junctional rearrangements at the wound margin. We used in vivo time-lapse quantitative microscopy to show that clathrin, dynamin, and the ADP-ribosylation factor 6, three components of the endocytic machinery, accumulate around wounds in Drosophila melanogaster embryos in a process that requires calcium signaling and actomyosin contractility. Blocking endocytosis with pharmacological or genetic approaches disrupted wound repair. The defect in wound closure was accompanied by impaired removal of E-cadherin from the wound edge and defective actomyosin cable assembly. E-cadherin overexpression also resulted in reduced actin accumulation around wounds and slower wound closure. Reducing E-cadherin levels in embryos in which endocytosis was blocked rescued actin localization to the wound margin. Our results demonstrate a central role for endocytosis in wound healing and indicate that polarized E-cadherin endocytosis is necessary for actomyosin remodeling during embryonic wound repair.

Indexed as

Actin CytoskeletonActomyosinADP-Ribosylation Factor 6ADP-Ribosylation FactorsAnimalsCadherinsCalcium SignalingCell MovementClathrinDrosophila melanogasterDynaminsEndocytosisEpitheliumGreen Fluorescent ProteinsMicroscopy, VideoTime-Lapse ImagingActomyosinADP-Ribosylation Factor 6ADP-Ribosylation FactorsCadherinsClathrinDynaminsGreen Fluorescent Proteins

Identifiers

PMID26304727
PMCPMC4555830
OpenAlexW1911021731

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.