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

Research output: Contribution to journalArticle

2 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 languageEnglish
Pages (from-to)2651-2658
Number of pages8
JournalMolecular Biology of the Cell
Volume30
Issue number21
DOIs
Publication statusPublished - 2019 Oct 1

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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