Rac function and regulation during Drosophila development

Satoko Hakeda-Suzuki, Julian Ng, Julia Tzu, Georg Dietzl, Yan Sun, Matthew Harms, Tim Nardine, Liqun Luo and Barry J. Dickson ()
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Satoko Hakeda-Suzuki: Research Institute of Molecular Pathology
Julian Ng: Stanford University
Julia Tzu: Stanford University
Georg Dietzl: Research Institute of Molecular Pathology
Yan Sun: Research Institute of Molecular Pathology
Matthew Harms: Stanford University
Tim Nardine: Stanford University
Liqun Luo: Stanford University
Barry J. Dickson: Research Institute of Molecular Pathology

Nature, 2002, vol. 416, issue 6879, 438-442

Abstract: Abstract Rac GTPases regulate the actin cytoskeleton to control changes in cell shape1,2. To date, the analysis of Rac function during development has relied heavily on the use of dominant mutant isoforms. Here, we use loss-of-function mutations to show that the three Drosophila Rac genes, Rac1, Rac2 and Mtl, have overlapping functions in the control of epithelial morphogenesis, myoblast fusion, and axon growth and guidance. They are not required for the establishment of planar cell polarity, as had been suggested on the basis of studies using dominant mutant isoforms3,4. The guanine nucleotide exchange factor, Trio, is essential for Rac function in axon growth and guidance, but not for epithelial morphogenesis or myoblast fusion. Different Rac activators thus act in different developmental processes. The specific cellular response to Rac activation may be determined more by the upstream activator than the specific Rac protein involved.

Date: 2002
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DOI: 10.1038/416438a

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