English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/41234
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:


A role for the chaperone Hsp70 in the regulation of border cell migration in the Drosophila ovary

AuthorsCobreros, Laura ; Fernández-Miñán, Ana ; Luque, Carlos M. ; González-Reyes, Acaimo ; Martín-Bermudo, María D.
Cell migration
PDGF/VEGF receptor
Protein binding
Issue Date31-Jul-2008
CitationMechanisms of Development 125(11-12): 1048-1058 (2008)
AbstractUnravelling the molecular mechanisms that govern cell migration is of great importance towards understanding both normal embryogenesis and physiological and pathological processes occurring in the adult. Migration of border cells (BCs) during Drosophila oogenesis provides a simple and attractive model in which to address this problem. Here, we show that the molecular chaperone Hsp70 is required for BC migration. Thus, BCs lacking all Hsp70 genes present in the fly genome fail to reorganize their actin cytoskeleton, resulting in migration defects. Similar defects are found when the Hsp70 co-chaperone DnaJ-1, the Drosophila homolog of the human Hsp40, is overexpressed specifically in BCs. In addition, we provide biochemical and genetic evidence for an interaction between DnaJ-1 and PDGF/VEGF receptor (PVR), which is also required for actin-mediated BC migration. Furthermore, our results showing that PVR also interacts genetically with Hsp70 suggest that a mechanism by which the DnaJ-1/Hsp70 chaperone complex regulates BC migration is by modulating PVR function.
Description11 páginas, 6 figuras.
Publisher version (URL)http://dx.doi.org/10.1016/j.mod.2008.07.006
Appears in Collections:(CABD) Artículos
Files in This Item:
There are no files associated with this item.
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.