Cdc37 is essential for JNK pathway activation and wound closure in Drosophila

Chan Wool Lee; Young Chang Kwon; Youngbin Lee; Min Yoon Park; Kwang Min Choe

doi:10.1091/mbc.E18-12-0822

Cdc37 is essential for JNK pathway activation and wound closure in Drosophila

Chan Wool Lee, Young Chang Kwon, Youngbin Lee, Min Yoon Park, Kwang Min Choe

Department of Systems Biology

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

5 Citations (Scopus)

Abstract

Wound closure in the Drosophila larval epidermis mainly involves nonproliferative, endocyling epithelial cells. Consequently, it is largely mediated by cell growth and migration. We discovered that both cell growth and migration in Drosophila require the cochaperone-encoding gene cdc37. Larvae lacking cdc37 in the epidermis failed to close wounds, and the cells of the epidermis failed to change cell shape and polarize. Likewise, wound-induced cell growth was significantly reduced, and correlated with a reduction in the size of the cell nucleus. The c-Jun N-terminal kinase (JNK) pathway, which is essential for wound closure, was not typically activated in injured cdc37 knockdown larvae. In addition, JNK, Hep, Mkk4, and Tak1 protein levels were reduced, consistent with previous reports showing that Cdc37 is important for the stability of various client kinases. Protein levels of the integrin β subunit and its wound-induced protein expression were also reduced, reflecting the disruption of JNK activation, which is crucial for expression of integrin β during wound closure. These results are consistent with a role of Cdc37 in maintaining the stability of the JNK pathway kinases, thus mediating cell growth and migration during Drosophila wound healing.

Original language	English
Pages (from-to)	2651-2658
Number of pages	8
Journal	Molecular Biology of the Cell
Volume	30
Issue number	21
DOIs	https://doi.org/10.1091/mbc.E18-12-0822
Publication status	Published - 2019 Oct 1

Bibliographical note

Funding Information:
We thank J. Ng, Y. Miyata, N. Silverman, B. Stronach, M. Therrien, The Bloomington Stock Center, The National Institute of Genetics in Japan, and The Vienna Drosophila Resource Center for fly stocks and antibodies. We are also very grateful to our colleagues in the laboratory for helpful discussions. This work was supported by a National Research Foundation of Korea grant funded by the Korean Government, Ministry of Science and ICT (Grant no. 2015R1A2A2A01006660) to K.-M.C.

Publisher Copyright:
© 2019 Lee et al.

All Science Journal Classification (ASJC) codes

Molecular Biology
Cell Biology

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10.1091/mbc.E18-12-0822

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title = "Cdc37 is essential for JNK pathway activation and wound closure in Drosophila",

abstract = "Wound closure in the Drosophila larval epidermis mainly involves nonproliferative, endocyling epithelial cells. Consequently, it is largely mediated by cell growth and migration. We discovered that both cell growth and migration in Drosophila require the cochaperone-encoding gene cdc37. Larvae lacking cdc37 in the epidermis failed to close wounds, and the cells of the epidermis failed to change cell shape and polarize. Likewise, wound-induced cell growth was significantly reduced, and correlated with a reduction in the size of the cell nucleus. The c-Jun N-terminal kinase (JNK) pathway, which is essential for wound closure, was not typically activated in injured cdc37 knockdown larvae. In addition, JNK, Hep, Mkk4, and Tak1 protein levels were reduced, consistent with previous reports showing that Cdc37 is important for the stability of various client kinases. Protein levels of the integrin β subunit and its wound-induced protein expression were also reduced, reflecting the disruption of JNK activation, which is crucial for expression of integrin β during wound closure. These results are consistent with a role of Cdc37 in maintaining the stability of the JNK pathway kinases, thus mediating cell growth and migration during Drosophila wound healing.",

author = "Lee, {Chan Wool} and Kwon, {Young Chang} and Youngbin Lee and Park, {Min Yoon} and Choe, {Kwang Min}",

note = "Funding Information: We thank J. Ng, Y. Miyata, N. Silverman, B. Stronach, M. Therrien, The Bloomington Stock Center, The National Institute of Genetics in Japan, and The Vienna Drosophila Resource Center for fly stocks and antibodies. We are also very grateful to our colleagues in the laboratory for helpful discussions. This work was supported by a National Research Foundation of Korea grant funded by the Korean Government, Ministry of Science and ICT (Grant no. 2015R1A2A2A01006660) to K.-M.C. Publisher Copyright: {\textcopyright} 2019 Lee et al.",

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AU - Lee, Chan Wool

AU - Kwon, Young Chang

AU - Lee, Youngbin

AU - Park, Min Yoon

AU - Choe, Kwang Min

N1 - Funding Information: We thank J. Ng, Y. Miyata, N. Silverman, B. Stronach, M. Therrien, The Bloomington Stock Center, The National Institute of Genetics in Japan, and The Vienna Drosophila Resource Center for fly stocks and antibodies. We are also very grateful to our colleagues in the laboratory for helpful discussions. This work was supported by a National Research Foundation of Korea grant funded by the Korean Government, Ministry of Science and ICT (Grant no. 2015R1A2A2A01006660) to K.-M.C. Publisher Copyright: © 2019 Lee et al.

PY - 2019/10/1

Y1 - 2019/10/1

N2 - Wound closure in the Drosophila larval epidermis mainly involves nonproliferative, endocyling epithelial cells. Consequently, it is largely mediated by cell growth and migration. We discovered that both cell growth and migration in Drosophila require the cochaperone-encoding gene cdc37. Larvae lacking cdc37 in the epidermis failed to close wounds, and the cells of the epidermis failed to change cell shape and polarize. Likewise, wound-induced cell growth was significantly reduced, and correlated with a reduction in the size of the cell nucleus. The c-Jun N-terminal kinase (JNK) pathway, which is essential for wound closure, was not typically activated in injured cdc37 knockdown larvae. In addition, JNK, Hep, Mkk4, and Tak1 protein levels were reduced, consistent with previous reports showing that Cdc37 is important for the stability of various client kinases. Protein levels of the integrin β subunit and its wound-induced protein expression were also reduced, reflecting the disruption of JNK activation, which is crucial for expression of integrin β during wound closure. These results are consistent with a role of Cdc37 in maintaining the stability of the JNK pathway kinases, thus mediating cell growth and migration during Drosophila wound healing.

AB - Wound closure in the Drosophila larval epidermis mainly involves nonproliferative, endocyling epithelial cells. Consequently, it is largely mediated by cell growth and migration. We discovered that both cell growth and migration in Drosophila require the cochaperone-encoding gene cdc37. Larvae lacking cdc37 in the epidermis failed to close wounds, and the cells of the epidermis failed to change cell shape and polarize. Likewise, wound-induced cell growth was significantly reduced, and correlated with a reduction in the size of the cell nucleus. The c-Jun N-terminal kinase (JNK) pathway, which is essential for wound closure, was not typically activated in injured cdc37 knockdown larvae. In addition, JNK, Hep, Mkk4, and Tak1 protein levels were reduced, consistent with previous reports showing that Cdc37 is important for the stability of various client kinases. Protein levels of the integrin β subunit and its wound-induced protein expression were also reduced, reflecting the disruption of JNK activation, which is crucial for expression of integrin β during wound closure. These results are consistent with a role of Cdc37 in maintaining the stability of the JNK pathway kinases, thus mediating cell growth and migration during Drosophila wound healing.

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Cdc37 is essential for JNK pathway activation and wound closure in Drosophila

Abstract

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