|Title||Regulation of armadillo by a Drosophila APC inhibits neuronal apoptosis during retinal development.|
|Publication Type||Journal Article|
|Year of Publication||1998|
|Authors||Ahmed, Y, Hayashi, S, Levine, A, Wieschaus, E|
|Date Published||1998 Jun 26|
|Keywords||Adenomatous Polyposis Coli Protein, Animals, Apoptosis, Armadillo Domain Proteins, beta Catenin, Cytoskeletal Proteins, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Gene Expression Regulation, Developmental, Genes, APC, Insect Proteins, Mutation, Photoreceptor Cells, Invertebrate, Proto-Oncogene Proteins, Repetitive Sequences, Nucleic Acid, Repressor Proteins, Retina, Retinal Degeneration, Signal Transduction, Trans-Activators, Transcription Factors, Wnt1 Protein|
We find that inactivation of a Drosophila homolog of the tumor suppressor APC (D-APC) causes retinal neuronal degeneration and pigment cell hypertrophy, a phenotype remarkably similar to that found in humans with germline APC mutations. Retinal degeneration in the D-APC mutant results from apoptotic cell death, which accompanies a defect in neuronal differentiation. Reduction in the Drosophila beta-catenin, Armadillo (Arm), rescues the differentiation defect and prevents apoptosis in the D-APC mutant, while Arm overexpression mimics D-APC inactivation. A mutation in dTCF, the DNA-binding protein required in Arm-mediated signal transduction, can eliminate the cell death without rescuing the differentiation defect in D-APC mutants. Uncoupling of these two Arm-induced processes suggests a novel role for the Arm/dTCF complex in the activation of apoptosis.