Abstract
BackgroundThe Focal Adhesion Kinase is a well studied tyrosine kinase involved in a wide number of cellular processes including cell adhesion and migration. It has also been shown to play important roles during embryonic development and targeted disruption of the FAK gene in mice results in embryonic lethality by day 8.5.Principal FindingsHere we examined the pattern of phosphorylation of FAK during Xenopus development and found that FAK is phosphorylated on all major tyrosine residues examined from early blastula stages well before any morphogenetic movements take place. We go on to show that FRNK fails to act as a dominant negative in the context of the early embryo and that the FERM domain has a major role in determining FAK’s localization at the plasma membrane. Finally, we show that autonomous expression of the FERM domain leads to the activation of endogenous FAK in a tyrosine 397 dependent fashion.ConclusionsOverall, our data suggest an important role for the FERM domain in the activation of FAK and indicate that integrin signalling plays a limited role in the in vivo activation of FAK at least during the early stages of development.
Highlights
Cell adhesion and migration are essential processes for embryonic development, wound healing and inflammation
Overall, our data suggest an important role for the FERM domain in the activation of Focal Adhesion Kinase (FAK) and indicate that integrin signalling plays a limited role in the in vivo activation of FAK at least during the early stages of development
Increased levels of expression and phosphorylation of FAK were observed during gastrulation indicating that FAK may be involved in regulating embryonic cell adhesive behaviour and morphogenesis [31,32]
Summary
Cell adhesion and migration are essential processes for embryonic development, wound healing and inflammation. The Focal Adhesion Kinase (FAK) is a 125-kDa nonreceptor tyrosine kinase that is recruited to focal adhesions and shown to be activated by integrin signalling [3]. As a key mediator of cell-ECM signalling, FAK has an important role in cell adhesion and migration, yet our understanding of the regulation of its activity in these processes remains incomplete [4,5,6]. The study of FAK has for a long time primarily focused on its role in cell adhesion and cell migration and as a result a lot of research has been carried out regarding the ways FAK becomes activated downstream of integrin signalling. The Focal Adhesion Kinase is a well studied tyrosine kinase involved in a wide number of cellular processes including cell adhesion and migration. It has been shown to play important roles during embryonic development and targeted disruption of the FAK gene in mice results in embryonic lethality by day 8.5
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