|Title||Patterned gene expression directs bipolar planar polarity in Drosophila.|
|Publication Type||Journal Article|
|Year of Publication||2004|
|Authors||Zallen, JA, Wieschaus, E|
|Date Published||2004 Mar|
|Keywords||Animals, Animals, Genetically Modified, Antigens, CD, Armadillo Domain Proteins, Body Patterning, Carrier Proteins, Cell Adhesion Molecules, Cell Movement, Cell Polarity, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Embryo, Nonmammalian, Embryonic Induction, Female, Gene Expression Regulation, Genes, Insect, Glycoproteins, Homeodomain Proteins, Immunoglobulins, Immunohistochemistry, Intracellular Signaling Peptides and Proteins, Male, Mutation, Myosin Type II, Nuclear Proteins, Receptors, Cell Surface, Trans-Activators, Transcription Factors|
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.
|Alternate Journal||Dev. Cell|