English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/43707
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

Integrin-dependent activation of the JNK signaling pathway by mechanical stress

AuthorsPereira, Andrea Maria; Tudor, Cicerone; Kanger, Johannes S.; Subramaniam, Vinod; Martín-Blanco, Enrique
Issue Date13-Dec-2011
PublisherPublic Library of Science
CitationPLoS ONE 6(12): e26182 (2011)
AbstractMechanical force is known to modulate the activity of the Jun N-terminal kinase (JNK) signaling cascade. However, the effect of mechanical stresses on JNK signaling activation has previously only been analyzed by in vitro detection methods. It still remains unknown how living cells activate the JNK signaling cascade in response to mechanical stress and what its functions are in stretched cells. We assessed in real-time the activity of the JNK pathway in Drosophila cells by Fluorescence Lifetime Imaging Microscopy (FLIM), using an intramolecular phosphorylation-dependent dJun-FRET (Fluorescence Resonance Energy Transfer) biosensor. We found that quantitative FRET-FLIM analysis and confocal microscopy revealed sustained dJun-FRET biosensor activation and stable morphology changes in response to mechanical stretch for Drosophila S2R+ cells. Further, these cells plated on different substrates showed distinct levels of JNK activity that associate with differences in cell morphology, integrin expression and focal adhesion organization. These data imply that alterations in the cytoskeleton and matrix attachments may act as regulators of JNK signaling, and that JNK activity might feed back to modulate the cytoskeleton and cell adhesion. We found that this dynamic system is highly plastic; at rest, integrins at focal adhesions and talin are key factors suppressing JNK activity, while multidirectional static stretch leads to integrin-dependent, and probably talin-independent, Jun sensor activation. Further, our data suggest that JNK activity has to coordinate with other signaling elements for the regulation of the cytoskeleton and cell shape remodeling associated with stretch.
Publisher version (URL)http://dx.doi.org/10.1371/journal.pone.0026182
URIhttp://hdl.handle.net/10261/43707
DOI10.1371/journal.pone.0026182
ISSN1932-6203
Appears in Collections:(IBMB) Artículos
Files in This Item:
File Description SizeFormat 
Integrin-Dependent.pdf3,16 MBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.