Evidence map›Paper›PMID 30202062›Full record

ArticleNature communications2018

AIP1 and cofilin ensure a resistance to tissue tension and promote directional cell rearrangement.

Keisuke Ikawa, Kaoru Sugimura

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 34 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

2 authors at 1 institution in 1 country.

Keisuke IkawaInstitute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University, Kyoto, 606-8501, Japan.
Kaoru SugimuraInstitute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University, Kyoto, 606-8501, Japan. ksugimura@icems.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-3076-7347
Kyoto University · JP

Funding

Japan Agency for Medical Research and Development (AMED) JP17gm5810025Japan Science and Technology Agency (JST) JPMJPR13A4Japan Society for the Promotion of Science (JSPS) 15H01321Japan Society for the Promotion of Science (JSPS) 17K15125
6 · The paper itself

Abstract

In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement. Here, we address the question in the Drosophila wing epithelium, where anisotropic tissue tension orients cell rearrangements. We found that anisotropic tissue tension localizes actin interacting protein 1 (AIP1), a cofactor of cofilin, on the remodeling junction via cooperative binding of cofilin to F-actin. AIP1 and cofilin promote actin turnover and locally regulate the Canoe-mediated linkage between actomyosin and the junction. This mechanism is essential for cells to resist the mechanical load imposed on the remodeling junction perpendicular to the direction of tissue stretching. Thus, the present study delineates how AIP1 and cofilin achieve an optimal balance between resistance to tissue tension and morphogenesis.

Indexed as

Actin CytoskeletonActinsAnimalsAnimals, Genetically ModifiedCell MovementDrosophila melanogasterDrosophila ProteinsEpithelial CellsEpitheliumIntercellular JunctionsMechanical PhenomenaMicrofilament ProteinsMicroscopy, ConfocalProtein BindingTime-Lapse ImagingWings, AnimalActinsALIX protein, DrosophilaDrosophila ProteinsMicrofilament Proteinstsr protein, Drosophila

Identifiers

PMID30202062
PMCPMC6131156
OpenAlexW2887896991

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.