Focal adhesion kinase controls morphogenesis of the Drosophila optic stalk
Focal adhesion kinase controls morphogenesis of the Drosophila optic stalk
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DOI：
10.1242/dev.001529
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发表时间：
2007-04-15
期刊：
影响因子：
4.6
通讯作者：
Tabata, Tetsuya
中科院分区：
文献类型：
--
作者：
Murakami, Satoshi;Umetsu, Daiki;Tabata, Tetsuya
在果蝇大脑中，感光细胞轴突（R轴突）通过管状视柄支配视神经节。该结构由表面胶质细胞（SG）组成，独立于R轴突投射形成。在参与视柄形成的基因筛选中，我们发现Fak56D编码哺乳动物局灶黏附激酶（FAK）的果蝇同源物。FAK是局灶黏附信号的主要组成部分，它调节各种细胞事件，包括细胞迁移和形态。我们发现Fak56D突变导致视柄结构严重破坏。Fak56D转基因表达在SG细胞中完全恢复了这些表型，而在光感受器细胞中则没有。此外，Fak56D基因与myospheroid相互作用，后者编码整合素β亚基。此外，我们发现CdGAPr也是视柄形成所必需的，并与Fak56D基因相互作用。CdGAPr编码一个与哺乳动物CdGAP同源的gtpase激活域，在局灶黏附信号传导中起作用。因此，视柄是一个简单的单层结构，可以作为研究胶质细胞形态发生和局灶黏附信号的发育作用的理想系统。
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 beta 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.