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dc.contributor.authorRichier, Benjaminen
dc.contributor.authorInoue, Yoshikoen
dc.contributor.authorDobramysl, Ulrichen
dc.contributor.authorFriedlander, Jonathanen
dc.contributor.authorBrown, Nicholasen
dc.contributor.authorGallop, Jenniferen
dc.date.accessioned2018-12-18T12:05:21Z
dc.date.available2018-12-18T12:05:21Z
dc.date.issued2018-08-16en
dc.identifier.issn0021-9533
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/287140
dc.description.abstractCells need to sense their environment to ensure accurate targeting to specific destinations. This occurs in developing muscles, which need to attach to tendon cells before muscle contractions can begin. Elongating myotube tips form filopodia, which are presumed to have sensory roles, and are later suppressed upon building the attachment site. Here, we use live imaging and quantitative image analysis of lateral transverse (LT) myotubes in Drosophila to show that filopodia suppression occurs as a result of integrin signaling. Loss of the integrin subunits PS2 and PS increased filopodia number and length at stages when they are normally suppressed. Conversely, inducing integrin signaling, achieved by expression of constitutively dimerised PS cytoplasmic domain (di), prematurely suppressed filopodia. We discovered that the integrin signal is transmitted through the protein Git (G-protein receptor coupled interacting protein) and its downstream kinase Pak (p21-activated kinase). Absence of these proteins causes profuse filopodia and prevents filopodial inhibition by di. Thus, integrin signaling terminates the exploratory behaviour of myotubes seeking tendons, enabling the actin machinery to focus on forming a strong attachment and assembling the contractile apparatus.
dc.languageengen
dc.publisherThe Company of Biologists Ltd.
dc.rightsAttribution 4.0 International
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleIntegrin signaling downregulates filopodia in muscle-tendon attachmenten
dc.typeArticle
prism.issueIdentifier16en
prism.numberjcs217133en
prism.publicationDate2018en
prism.publicationNameJournal of Cell Scienceen
prism.volume131en
dc.identifier.doi10.17863/CAM.34447
dcterms.dateAccepted2018-07-12en
rioxxterms.versionofrecord10.1242/jcs.217133en
rioxxterms.versionVoR*
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/en
rioxxterms.licenseref.startdate2018-08-16en
dc.contributor.orcidDobramysl, Ulrich [0000-0001-9363-654X]
dc.contributor.orcidBrown, Nicholas [0000-0002-8958-7017]
dc.contributor.orcidGallop, Jennifer [0000-0002-9978-1382]
dc.identifier.eissn1477-9137
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idEuropean Research Council (281971)
pubs.funder-project-idWELLCOME TRUST (105602/Z/14/Z)
pubs.funder-project-idWellcome Trust (095829/Z/11/Z)
pubs.funder-project-idWellcome Trust (086451/Z/08/Z)
pubs.funder-project-idWellcome Trust (069943/Z/02/Z)
pubs.funder-project-idWellcome Trust (092096/Z/10/Z)
pubs.funder-project-idCancer Research UK (A14492)
cam.issuedOnline2018-07-27en
dc.identifier.urlhttp://jcs.biologists.org/content/131/16/jcs217133en


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International