aPKC controls microtubule organization to balance adherens junction symmetry and planar polarity during development

Dev Cell. 2007 May;12(5):727-38. doi: 10.1016/j.devcel.2007.02.011.

Abstract

Tissue morphogenesis requires assembling and disassembling individual cell-cell contacts without losing epithelial integrity. This requires dynamic control of adherens junction (AJ) positioning around the apical domain, but the mechanisms involved are unclear. We show that atypical Protein Kinase C (aPKC) is required for symmetric AJ positioning during Drosophila embryogenesis. aPKC is dispensable for initial apical AJ recruitment, but without aPKC, AJs form atypical planar-polarized puncta at gastrulation. Preceding this, microtubules fail to dissociate from centrosomes, and at gastrulation abnormally persistent centrosomal microtubule asters cluster AJs into the puncta. Dynein enrichment at the puncta suggests it may draw AJs and microtubules together and microtubule disruption disperses the puncta. Through cytoskeletal disruption in wild-type embryos, we find a balance of microtubule and actin interactions controls AJ symmetry versus planar polarity during normal gastrulation. aPKC apparently regulates this balance. Without aPKC, abnormally strong microtubule interactions break AJ symmetry and epithelial structure is lost.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Adherens Junctions / metabolism*
  • Animals
  • Cell Polarity*
  • Centrosome / metabolism
  • Drosophila Proteins / metabolism
  • Drosophila melanogaster / cytology*
  • Drosophila melanogaster / embryology*
  • Drosophila melanogaster / enzymology
  • Embryo, Nonmammalian / cytology
  • Embryo, Nonmammalian / metabolism
  • Epithelium
  • Gastrula / cytology
  • Gastrula / metabolism
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Microtubules / enzymology*
  • Mutant Proteins / metabolism
  • Mutation / genetics
  • Protein Kinase C / metabolism*

Substances

  • Actins
  • Drosophila Proteins
  • Intracellular Signaling Peptides and Proteins
  • Mutant Proteins
  • baz protein, Drosophila
  • PKC-3 protein
  • Protein Kinase C