Focal adhesion kinase controls morphogenesis of the Drosophila optic stalk

Satoshi Murakami, Daiki Umetsu, Yuko Maeyama, Makoto Sato, Shoko Yoshida, Tetsuya Tabata

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


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 woe 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 β 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.

Original languageEnglish
Pages (from-to)1539-1548
Number of pages10
Issue number8
Publication statusPublished - 2007 Apr
Externally publishedYes


  • CdGAPr
  • Drosophila
  • Fak56D
  • Glia
  • Optic stalk

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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