Requirement for Pak3 in Rac1-induced organization of actin and myosin during Drosophila larval wound healing

Seung Hee Baek; Hae Weon Cho; Young Chang Kwon; Ji Hyun Lee; Moon Jong Kim; Hyangkyu Lee; Kwang Min Choe

doi:10.1016/j.febslet.2012.01.061

Requirement for Pak3 in Rac1-induced organization of actin and myosin during Drosophila larval wound healing

Seung Hee Baek, Hae Weon Cho, Young Chang Kwon, Ji Hyun Lee, Moon Jong Kim, Hyangkyu Lee, Kwang Min Choe

Research output: Contribution to journal › Article › peer-review

21 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	772-777
Number of pages	6
Journal	FEBS Letters
Volume	586
Issue number	6
DOIs	https://doi.org/10.1016/j.febslet.2012.01.061
Publication status	Published - 2012 Mar 23

Bibliographical note

Funding 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

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2012.01.061

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title = "Requirement for Pak3 in Rac1-induced organization of actin and myosin during Drosophila larval wound healing",

abstract = "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.",

author = "Baek, {Seung Hee} and Cho, {Hae Weon} and Kwon, {Young Chang} and Lee, {Ji Hyun} and Kim, {Moon Jong} and Hyangkyu Lee and Choe, {Kwang Min}",

note = "Funding 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). ",

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AU - Kwon, Young Chang

AU - Lee, Ji Hyun

AU - Kim, Moon Jong

AU - Lee, Hyangkyu

AU - Choe, Kwang Min

N1 - Funding 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).

PY - 2012/3/23

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N2 - 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.

AB - 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.

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Requirement for Pak3 in Rac1-induced organization of actin and myosin during Drosophila larval wound healing

Abstract

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