Regulation of Armadillo by a Drosophila APC inhibits neuronal apoptotis during retinal development

Yashi Ahmed, Shigemi Hayashi, Arnold Levine, Eric Wieschaus

Research output: Contribution to journalArticlepeer-review

187 Scopus citations

Abstract

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 β-catenin, Armadillo (Arm), rescues the differentiation defect and prevents apoptosis in the D-APC mutant, while Arm overexpression mimics D-APC inactivation. A mutation if 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.

Original languageEnglish (US)
Pages (from-to)1171-1182
Number of pages12
JournalCell
Volume93
Issue number7
DOIs
StatePublished - Jun 26 1998

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

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