FGF coordinates air sac development by activation of the EGF ligand Vein through the transcription factor PntP2
How several signaling pathways are coordinated to generate complex organs through regulation of tissue growth and patterning is a fundamental question in developmental biology. The larval trachea of Drosophila is composed of differentiated functional cells and groups of imaginal tracheoblasts that b...
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Published in | Scientific reports Vol. 5; no. 1; p. 17806 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
03.12.2015
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Summary: | How several signaling pathways are coordinated to generate complex organs through regulation of tissue growth and patterning is a fundamental question in developmental biology. The larval trachea of
Drosophila
is composed of differentiated functional cells and groups of imaginal tracheoblasts that build the adult trachea during metamorphosis. Air sac primordium cells (ASP) are tracheal imaginal cells that form the dorsal air sacs that supply oxygen to the flight muscles of the
Drosophila
adult. The ASP emerges from the tracheal branch that connects to the wing disc by the activation of both Bnl-FGF/Btl and EGFR signaling pathways. Together, these pathways promote cell migration and proliferation. In this study we demonstrate that Vein (
vn
) is the EGF ligand responsible for the activation of the EGFR pathway in the ASP. We also find that the Bnl-FGF/Btl pathway regulates the expression of
vn
through the transcription factor PointedP2 (PntP2). Furthermore, we show that the FGF target gene
escargot (esg)
attenuates EGFR signaling at the tip cells of the developing ASP, reducing their mitotic rate to allow proper migration. Altogether, our results reveal a link between Bnl-FGF/Btl and EGFR signaling and provide novel insight into how the crosstalk of these pathways regulates migration and growth. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Present address: University of Texas MD Anderson Cancer Center Houston, Texas, United States. |
ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/srep17806 |