Epithelial pathway revealed

"In nature, different organisms sculpt epithelial sheets into a bewildering array of forms, but relatively little is known about the mechanisms involved," co-author Matthew Gibson of Harvard University told The Scientist. "This pathway or related ones could perhaps have conserved function in epithelial morphogenesis in other organismal systems."Gibson and senior coauthor Norbert Perrimon screened for genetic factors that control epithelial cell shape during Drosophila wing development. They used a tissue-specific Gal4 driver to direct expression of flipase in wing epithelia at different stages of development. This catalyzed mitotic recombination between a mutagenized chromatid bearing a flipase recombination target and its green-fluorescent protein (GFP) tagged homolog, producing both a homozygous mutant GFP-negative cell and a paired cell bearing two copies of GFP.One experimental line developed defects in establishing or maintaining pseudostratified columnar shape in medial regions of the wing imaginal disc, resulting in cystlike epithelial extrusions. Recombination mapping against a set of P-element insertions pinpointed the mutation to cytological interval 25D-25F, which bears the decapentaplegic (DPP) receptor thickveins (tkv) crucial for imaginal disc development. Another mutant tkv allele and an allele of a downstream signal transducer mad12 led to extrusion as well, linking this phenotype to defective DPP signaling and not a unique effect of the allele identified in their study, dubbed tkv-extruded.Independently, Jie Shen and Christian Dahmann at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, investigated what role decapentaplegic (DPP) plays in wing epithelial cells. Prior experiments suggested DPP's role was to control cell survival, since reduced DPP signaling activated the JNK stress signaling pathway and apoptosis. Shen and Dahmann analyzed tkv jnk double mutants within developing wing epithelia via flipase recombin