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1 Department of Molecular Biosciences, University of Kansas, 5049 Haworth Hall, 1200 Sunnyside Avenue, Lawrence, KS 66045, USA
2 Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
3 Howard Hughes Medical Institute, Department of Anatomy Box 0452, University of California, San Francisco, CA 94143, USA
* These authors contributed equally to this work
Author for correspondence (e-mail: erikl{at}ku.edu)
Accepted August 21, 2001
The Caenorhabditis elegans genome contains three rac-like genes, ced-10, mig-2, and rac-2. We report that ced-10, mig-2 and rac-2 act redundantly in axon pathfinding: inactivating one gene had little effect, but inactivating two or more genes perturbed both axon outgrowth and guidance. mig-2 and ced-10 also have redundant functions in some cell migrations. By contrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtle roles in this process. Rac activators are also used differentially. The UNC-73 Trio Rac GTP exchange factor affected all Rac pathways in axon pathfinding and cell migration but did not affect cell-corpse phagocytosis. CED-5 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in axon pathfinding. Thus, distinct regulatory proteins modulate Rac activation and function in different developmental processes.
Key words: C. elegans, Rac, ced-10, mig-2, rac-2, Axon pathfinding, Cell migration, Phagocytosis
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