4.4 Article

Drosophila apc regulates delamination of invasive epithelial clusters

Journal

DEVELOPMENTAL BIOLOGY
Volume 368, Issue 1, Pages 76-85

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2012.05.017

Keywords

Border cell delamination; Apc; beta-catenin/Armadillo; DE-cadherin

Funding

  1. Center National de la Recherche Scientifique, Ministere de la Recherche et de l'Enseignement Superieur
  2. Indo-French Center for Promotion of Advanced Research
  3. Association pour la Recherche Contre le Cancer
  4. European Molecular Biology Organization Young Investigator Program
  5. Agence Nationale de la Recherche

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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 (Mac] or dapc2 expression. Loss of dapc1 function was associated with an abnormal lasting accumulation of beta-catenin/Armadillo and E-cadherin at the boundary between migrating border and stretched cells. Moreover, beta-catenin/armadillo or E-cadherin downregulation rescued the dapcl loss of function phenotype. Altogether these results indicate that Drosophila Apc1 is required for dynamic remodeling of beta-catenin/Armadillo and E-cadherin adhesive complexes between outer border cells and stretched cells regulating proper delamination and invasion of migrating epithelial clusters. (C) 2012 Elsevier Inc. All rights reserved.

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