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doi: 10.1242/10.1242/dev.00613
1 Departamento de Histologia e Embriologia, Universidade Federal do Rio de
Janeiro, 21941-970, Rio de Janeiro, Brazil
2 Section of Cell and Developmental Biology, University of California, San
Diego, La Jolla, CA 92093-0349, USA
* Author for correspondence (e-mail: haraujo{at}histo.ufrj.br)
Accepted 9 May 2003
Morphogenesis of the Drosophila wing depends on a series of
cell-cell and cell-extracellular matrix interactions. During pupal wing
development, two secreted proteins, encoded by the short gastrulation
(sog) and decapentaplegic (dpp) genes, vie to
position wing veins in the center of broad provein territories. Expression of
the Bmp4 homolog dpp in vein cells is counteracted by expression of
the Bmp antagonist sog in intervein cells, which results in the
formation of straight veins of precise width. We screened for genetic
interactions between sog and genes encoding a variety of
extracellular components and uncovered interactions between sog and
myospheroid (mys), multiple edematous wing
(mew) and scab (scb), which encode ßPS,
PS1 and PS3 integrin subunits, respectively. Clonal analysis
reveals that integrin mutations affect the trajectory of veins inside the
provein domain and/or their width and that misexpression of sog can
alter the behavior of cells in such clones. In addition, we show that a low
molecular weight form of Sog protein binds to PS1ßPS. We find that
Sog can diffuse from its intervein site of production into adjacent provein
domains, but only on the dorsal surface of the wing, where Sog interacts
functionally with integrins. Finally, we show that Sog diffusion into provein
regions and the reticular pattern of extracellular Sog distribution in
wild-type wings requires mys and mew function. We propose
that integrins act by binding and possibly regulating the
activity/availability of different forms of Sog during pupal development
through an adhesion independent mechanism.
Key words: Drosophila, Sog, Integins, Bmps
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