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Regulation of armadillo by a Drosophila APC inhibits neuronal apoptosis during retinal development.

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

Cell

journal_title

Cell

authors

Ahmed Y,Hayashi S,Levine A,Wieschaus E

doi

10.1016/s0092-8674(00)81461-0

subject

Has Abstract

pub_date

1998-06-26 00:00:00

pages

1171-82

issue

7

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(00)81461-0

journal_volume

93

pub_type

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