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 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.
journal_name
Celljournal_title
Cellauthors
Ahmed Y,Hayashi S,Levine A,Wieschaus Edoi
10.1016/s0092-8674(00)81461-0subject
Has Abstractpub_date
1998-06-26 00:00:00pages
1171-82issue
7eissn
0092-8674issn
1097-4172pii
S0092-8674(00)81461-0journal_volume
93pub_type
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