Genetics, Vol. 155, 1725-1740, August 2000, Copyright © 2000

A Screen for Mutations That Suppress the Phenotype of Drosophila armadillo, the ß-Catenin Homolog

Rachel T. Coxb, Donald G. McEwenc, Denise L. Mysterc, Robert J. Duroniob,c,a,d, Joseph Loureiroa, and Mark Peiferb,c,a
a Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599-3280
b Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, North Carolina 27599-3280
c Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-3280
d Program in Molecular Biology and Biotechnology, University of North Carolina, Chapel Hill, North Carolina 27599-3280

Corresponding author: Mark Peifer, Biology, CB#3280, University of North Carolina, Chapel Hill, NC 27599-3280., peifer{at}unc.edu (E-mail)

Communicating editor: K. ANDERSON

During development signaling pathways coordinate cell fates and regulate the choice between cell survival or programmed cell death. The well-conserved Wingless/Wnt pathway is required for many developmental decisions in all animals. One transducer of the Wingless/Wnt signal is Armadillo/ß-catenin. Drosophila Armadillo not only transduces Wingless signal, but also acts in cell-cell adhesion via its role in the epithelial adherens junction. While many components of both the Wingless/Wnt signaling pathway and adherens junctions are known, both processes are complex, suggesting that unknown components influence signaling and junctions. We carried out a genetic modifier screen to identify some of these components by screening for mutations that can suppress the armadillo mutant phenotype. We identified 12 regions of the genome that have this property. From these regions and from additional candidate genes tested we identified four genes that suppress arm: dTCF, puckered, head involution defective (hid), and Dpresenilin. We further investigated the interaction with hid, a known regulator of programmed cell death. Our data suggest that Wg signaling modulates Hid activity and that Hid regulates programmed cell death in a dose-sensitive fashion.





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