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The Drosophila ribbon gene encodes a nuclear BTB domain protein that promotes epithelial migration and morphogenesis

Katherine Shim¹, Kimberly J. Blake^2,*, Joseph Jack^2, and Mark A. Krasnow^1,

¹ Howard Hughes Medical Institute and Department of Biochemistry, Stanford University, Stanford, CA 94305-5307, USA
² Department of Anatomy, University of Connecticut Health Center, Farmington, CT 06030, USA
^* Present address: Mitchell College, New London, CT 06320, USA
Present address: 9 Cricket Lane, Simsbury, CT 06070, USA

Author for correspondence (e-mail: krasnow{at}cmgm.stanford.edu)

Accepted September 10, 2001

During development of the Drosophila tracheal (respiratory) system, the cell bodies and apical and basal surfaces of the tracheal epithelium normally move in concert as new branches bud and grow out to form tubes. We show that mutations in the Drosophila ribbon (rib) gene disrupt this coupling: the basal surface continues to extend towards its normal targets, but movement and morphogenesis of the tracheal cell bodies and apical surface is severely impaired, resulting in long basal membrane protrusions but little net movement or branch formation. rib mutant tracheal cells are still responsive to the Branchless fibroblast growth factor (FGF) that guides branch outgrowth, and they express apical membrane markers normally. This suggests that the defect lies either in transmission of the FGF signal from the basal surface to the rest of the cell or in the apical cell migration and tubulogenesis machinery. rib encodes a nuclear protein with a BTB/POZ domain and Pipsqueak DNA-binding motif. It is expressed in the developing tracheal system and other morphogenetically active epithelia, many of which are also affected in rib mutants. We propose that Rib is a key regulator of epithelial morphogenesis that promotes migration and morphogenesis of the tracheal cell bodies and apical surface and other morphogenetic movements.

Key words: Drosophila, ribbon, BTB/POZ domain, Pipsqueak domain, Trachea, Branching morphogenesis, FGF, Epithelial migration

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