@article{86386,
  keywords = {Animals, Immunohistochemistry, Drosophila, Gene Expression Regulation, Mutation, Transcription Factors, Trans-Activators, Receptors, Cell Surface, Carrier Proteins, DNA-Binding Proteins, Female, Male, Nuclear Proteins, Body Patterning, Embryo, Nonmammalian, Cell Movement, Animals, Genetically Modified, Homeodomain Proteins, Cell Adhesion Molecules, Intracellular Signaling Peptides and Proteins, Drosophila Proteins, Cell Polarity, Genes, Insect, Antigens, CD, Immunoglobulins, Myosin Type II, Armadillo Domain Proteins, Embryonic Induction, Glycoproteins, Signaling Lymphocytic Activation Molecule Family Member 1},
  author = {Jennifer Zallen and Eric Wieschaus},
  title = {Patterned gene expression directs bipolar planar polarity in Drosophila.},
  abstract = { During convergent extension in Drosophila, polarized cell movements cause the germband to narrow along the dorsal-ventral (D-V) axis and more than double in length along the anterior-posterior (A-P) axis. This tissue remodeling requires the correct patterning of gene expression along the A-P axis, perpendicular to the direction of cell movement. Here, we demonstrate that A-P patterning information results in the polarized localization of cortical proteins in intercalating cells. In particular, cell fate differences conferred by striped expression of the even-skipped and runt pair-rule genes are both necessary and sufficient to orient planar polarity. This polarity consists of an enrichment of nonmuscle myosin II at A-P cell borders and Bazooka/PAR-3 protein at the reciprocal D-V cell borders. Moreover, bazooka mutants are defective for germband extension. These results indicate that spatial patterns of gene expression coordinate planar polarity across a multicellular population through the localized distribution of proteins required for cell movement. },
  year = {2004},
  journal = {Dev Cell},
  volume = {6},
  pages = {343-55},
  month = {03/2004},
  issn = {1534-5807},
  language = {eng},
}