Rho-family small GTPases regulate epithelial cell sheet migration by organizing actin and myosin during wound healing. Here, we report that Pak3, but not Pak1, is a downstream target protein for Rac1 in wound closure of the Drosophila larval epidermis. Pak3-deficient larvae failed to close a wound hole and this defect was not rescued by Pak1 expression, indicating differential functions of the two proteins. Pak3 localized to the wound margin, which selectively required Rac1. Pak3-deficient larvae showed severe defects in actin-myosin organization at the wound margin and in submarginal cells, which was reminiscent of the phenotypes of Rac1-deficient larvae. These results suggest that Pak3 specifically mediates Rac1 signaling in organizing actin and myosin during Drosophila epidermal wound healing.
Bibliographical noteFunding Information:
We thank the Bloomington Stock Center, N. Harden, and G. Bashaw for fly stocks and antibodies. We are grateful to members of the Choe lab for helpful discussions on the project. S.H.B., H.W.C., Y.-C.K., J.H.L., and M.J.K. were supported by Brain Korea 21, and Y.-C.K. and J.H.L. were additionally supported by a Seoul Science Fellowship. This research was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology ( 2009-0077495 to H.K.L. and 2011-0005000 to K.-M.C).
All Science Journal Classification (ASJC) codes
- Structural Biology
- Molecular Biology
- Cell Biology