|
|
|
|||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||

Abteilung Zellbiologie, Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland
* These authors contributed equally to this study
Author for correspondence (e-mail: markus.affolter{at}unibas.ch)
Accepted August 24, 2001
We wanted to investigate the relationship between receptor tyrosine kinase (RTK) activated signaling pathways and the induction of cell migration. Using Drosophila tracheal and mesodermal cell migration as model systems, we find that the intracellular domain of the fibroblast growth factor receptors (FGFRs) Breathless (Btl) and Heartless (Htl) can be functionally replaced by the intracellular domains of Torso (Tor) and epidermal growth factor receptor (EGFR). These hybrid receptors can also rescue cell migration in the absence of Downstream of FGFR (Dof), a cytoplasmic protein essential for FGF signaling. These results demonstrate that tracheal and mesodermal cells respond during a specific time window to a receptor tyrosine kinase (RTK) signal with directed migration, independent of the presence or absence of Dof. We discuss our findings in the light of the recent findings that RTKs generate a generic signal that is interpreted in responding cells according to their developmental history.
Key words: Cell migration, FGF signaling, Receptor tyrosine kinases, Trachea, Mesoderm, Drosophila
This article has been cited by other articles:
![]() |
C. D. Andl, T. Mizushima, H. Nakagawa, K. Oyama, H. Harada, K. Chruma, M. Herlyn, and A. K. Rustgi Epidermal Growth Factor Receptor Mediates Increased Cell Proliferation, Migration, and Aggregation in Esophageal Keratinocytes in Vitro and in Vivo J. Biol. Chem., January 10, 2003; 278(3): 1824 - 1830. [Abstract] [Full Text] [PDF] |
||||