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Updated: May 22, 2026

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
Published on: July 25, 2017
Drosophila apc regulates delamination of invasive epithelial clusters
F M De Graeve1, V Van de Bor, C Ghiglione
1Institut de Biologie Valrose, Université de Nice Sophia Antipolis, UMR CNRS 7277, UMR Inserm 1091, 28 Avenue Valrose, 06108 Nice Cedex 02, France.
Abstract:
Border Cells in the Drosophila ovaries are a useful genetic model for understanding the molecular events underlying epithelial cell motility. During stage 9 of egg chamber development they detach from neighboring stretched cells and migrate between the nurse cells to reach the oocyte. RNAi screening allowed us to identify the dapc1 gene as being critical in this process. Clonal and live analysis showed a requirement of dapc1 in both outer border cells and contacting stretched cells for delamination. This mutant phenotype was rescued by dapc1 or dapc2 expression. Loss of dapc1 function was associated with an abnormal lasting accumulation of β-catenin/Armadillo and E-cadherin at the boundary between migrating border and stretched cells. Moreover, β-catenin/armadillo or E-cadherin downregulation rescued the dapc1 loss of function phenotype. Altogether these results indicate that Drosophila Apc1 is required for dynamic remodeling of β-catenin/Armadillo and E-cadherin adhesive complexes between outer border cells and stretched cells regulating proper delamination and invasion of migrating epithelial clusters.
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