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  • Original Paper
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Ectopic expression of constitutively activated Ral GTPase inhibits cell shape changes during Drosophila eye development

Abstract

The small GTP-binding protein Ral is activated by RalGDS, one of the effector molecules for Ras. Active Ral binds to a GTPase activating protein for CDC42 and Rac. Although previous studies suggest a role for Ral in the regulation of CDC42 and Rac, which are involved in arranging the cytoskeleton, its in vivo function is largely unknown. To examine the effect of overexpressing Ral on development, transgenic Drosophila were generated that overexpress wild-type or mutated Ral during eye development. While wild-type Ral caused no developmental defects, expression of a constitutively activated protein resulted in a rough eye phenotype. Activated Ral did not affect cell fate determination in the larval eye discs but caused severe disruption of the ommatidial organization later in pupal development. Phalloidin staining showed that activated Ral perturbed the cytoskeletal structure and cell shape changes during pupal development. This phenotype is similar to that caused by RhoA overexpression. In addition, the phenotype was synergistically enhanced by the coexpression of RhoA. These results suggest that Ral functions to control the cytoskeletal structure required for cell shape changes during Drosophila development.

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Acknowledgements

We thank Kaoru Saigo, Seymor Benzer, Iswar Hariharan, Yuh Nung Jan, Tetsuya Kojima, Liqun Luo, Marek Mlodzik, Rick Fehon, Yasuyoshi Nishida, Gerald Rubin, the Developmental Studies Hybridoma Bank and the Bloomington Stock Center for the fly stocks and antibodies used in this study. We are grateful to Ritsuko Shimamura and Sachiyo Miyao for their help in maintenance of fly strains. This work was supported by grants from the Japan Ministry of Education, Science and Culture to KS, AK and HO.

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Sawamoto, K., Yamada, C., Kishida, S. et al. Ectopic expression of constitutively activated Ral GTPase inhibits cell shape changes during Drosophila eye development. Oncogene 18, 1967–1974 (1999). https://doi.org/10.1038/sj.onc.1202522

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