Kindlin-2 controls bidirectional signaling of integrins

Control of integrin activation is required for cell adhesion and ligand-induced signaling. Here we report that loss of the focal adhesion protein Kindlin-2 in mice results in peri-implantation lethality caused by severe detachment of the endoderm and epiblast from the basement membrane. We found tha...

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Bibliographic Details
Published inGenes & development Vol. 22; no. 10; pp. 1325 - 1330
Main Authors Montanez, Eloi, Ussar, Siegfried, Schifferer, Martina, Bösl, Michael, Zent, Roy, Moser, Markus, Fässler, Reinhard
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 15.05.2008
Subjects
Actins - metabolism
Animals
Blastocyst
Cell Adhesion - genetics
CHO Cells
Cricetinae
Cricetulus
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
Cytoskeletal Proteins - physiology
Embryo Loss - genetics
Embryo, Mammalian
Endoderm - physiology
Integrins - metabolism
Integrins - physiology
Mice
Mice, Knockout
Muscle Proteins - genetics
Muscle Proteins - metabolism
Muscle Proteins - physiology
Polymers - metabolism
Protein Binding
Research Communication
Signal Transduction - genetics
Talin - physiology
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Summary:Control of integrin activation is required for cell adhesion and ligand-induced signaling. Here we report that loss of the focal adhesion protein Kindlin-2 in mice results in peri-implantation lethality caused by severe detachment of the endoderm and epiblast from the basement membrane. We found that Kindlin-2-deficient cells were unable to activate their integrins and that Kindlin-2 is required for talin-induced integrin activation. Furthermore, we demonstrate that Kindlin-2 is required for integrin outside-in signaling to enable firm adhesion and spreading. Our findings provide evidence that Kindlin-2 is a novel and essential element of bidirectional integrin signaling.
Bibliography:ObjectType-Article-1
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These authors contributed equally to this work.
ISSN:0890-9369
1549-5477
DOI:10.1101/gad.469408