Rac GTPases act as molecular switch in various morphogenic events. However, the regulation of their activities during the development of multicellular organisms is not well understood. Caenorhabditis elegans rac genes
ced-10 and
mig-2 have been shown to act redundantly to control P cell migration and the axon outgrowth of D type motoneurons. We showed that
ced-10 and
mig-2 also control amphid axon outgrowth and amphid dendrite fasciculation in a redundant fashion. Our biochemical and genetic data indicate that
unc-73, which encodes a protein related to Trio-like guanine nucleotide exchange factor, acts as a direct activator of
ced-10 and
mig-2 during P cell migration and axon outgrowth of D type motoneurons and amphid sensory neurons. Furthermore, rac regulators
ced-2/crkII and
ced-5/dock180 function genetically upstream of
ced-10 and
mig-2 during axon outgrowth of D type motoneurons and act upstream of
mig-2 but not
ced-10 during P cell migration. However, neither
ced-2/crkII nor
ced-5/dock180 is involved in amphid axon outgrowth. Therefore, distinct rac regulators control
ced-10 and
mig-2 differentially in various cellular processes.