PTEN controls junction lengthening and stability during cell rearrangement in epithelial tissue

Dev Cell. 2013 Jun 10;25(5):534-46. doi: 10.1016/j.devcel.2013.04.020. Epub 2013 May 23.


Planar cell rearrangements control epithelial tissue morphogenesis and cellular pattern formation. They lead to the formation of new junctions whose length and stability determine the cellular pattern of tissues. Here, we show that during Drosophila wing development the loss of the tumor suppressor PTEN disrupts cell rearrangements by preventing the lengthening of newly formed junctions that become unstable and keep on rearranging. We demonstrate that the failure to lengthen and to stabilize is caused by the lack of a decrease of Myosin II and Rho-kinase concentration at the newly formed junctions. This defect results in a heterogeneous cortical contractility at cell junctions that disrupts regular hexagonal pattern formation. By identifying PTEN as a specific regulator of junction lengthening and stability, our results uncover how a homogenous distribution of cortical contractility along the cell cortex is restored during cell rearrangement to control the formation of epithelial cellular pattern.

Publication types

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

MeSH terms

  • Animals
  • Crosses, Genetic
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / embryology
  • Epithelial Cells / cytology
  • Epithelium / embryology*
  • Epithelium / pathology
  • Gene Expression Regulation, Developmental*
  • Green Fluorescent Proteins / metabolism
  • Intercellular Junctions / metabolism*
  • Morphogenesis
  • Mutation
  • Myosin Type II / metabolism
  • PTEN Phosphohydrolase / metabolism*
  • Wings, Animal / embryology*


  • Drosophila Proteins
  • Green Fluorescent Proteins
  • PTEN Phosphohydrolase
  • PTEN protein, Drosophila
  • Myosin Type II