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First published online 14 March 2007
doi: 10.1242/dev.001529

Development 134, 1539-1548 (2007)
Published by The Company of Biologists 2007
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Focal adhesion kinase controls morphogenesis of the Drosophila optic stalk

Satoshi Murakami1,2, Daiki Umetsu1,2, Yuko Maeyama1, Makoto Sato1,2, Shoko Yoshida1,2 and Tetsuya Tabata1,2,*

1 Laboratory of Morphogenesis, Institute of Molecular and Cellular Biosciences, the University of Tokyo, 1-1-1 Yayoi, Bunkyo-Ku, Tokyo 113-0032, Japan.
2 Graduate Program in Biophysics and Biochemistry, Graduate School of Science, the University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo 113-0033, Japan.

* Author for correspondence (e-mail: ttabata{at}iam.u-tokyo.ac.jp)

Accepted 8 February 2007

Photoreceptor cell axons (R axons) innervate optic ganglia in the Drosophila brain through the tubular optic stalk. This structure consists of surface glia (SG) and forms independently of R axon projection. In a screen for genes involved in optic stalk formation, we identified Fak56D encoding a Drosophila homolog of mammalian focal adhesion kinase (FAK). FAK is a main component of the focal adhesion signaling that regulates various cellular events, including cell migration and morphology. We show that Fak56D mutation causes severe disruption of the optic stalk structure. These phenotypes were completely rescued by Fak56D transgene expression in the SG cells but not in photoreceptor cells. Moreover, Fak56D genetically interacts with myospheroid, which encodes an integrin ß subunit. In addition, we found that CdGAPr is also required for optic stalk formation and genetically interacts with Fak56D. CdGAPr encodes a GTPase-activating domain that is homologous to that of mammalian CdGAP, which functions in focal adhesion signaling. Hence the optic stalk is a simple monolayered structure that can serve as an ideal system for studying glial cell morphogenesis and the developmental role(s) of focal adhesion signaling.

Key words: Fak56D, CdGAPr, Optic stalk, Glia, Drosophila




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