TY - JOUR
T1 - Regulation of Armadillo by a Drosophila APC inhibits neuronal apoptotis during retinal development
AU - Ahmed, Yashi
AU - Hayashi, Shigemi
AU - Levine, Arnold
AU - Wieschaus, Eric
N1 - Funding Information:
We thank Trudi Schüpbach, Ming Zhou, and Joe Goodhouse for much help with genetic screens, sequencing of the D-APC alleles, and confocal microscopy, respectively. We thank Claudio Pikielny, Yash Hiromi, Susanne Kramer, Trudi Schüpbach, Reba Samanta, and Tanya Wolff for suggestions throughout this work and Rachel Hoang, Maureen Murphy, Li-Mei Pai, Lifeng Xu, and Tom Vogt for suggestions on the manuscript. We thank Konrad Basler, Nancy Bonini, Bruce Hay, Mark Peifer, Benedicte Sanson, Esther Siegfried, Gary Struhl, and the Bloomington Stock Center for fly strains and the Developmental Studies Hybridoma Bank for the Neurotactin antibody. Y. A. is an HHMI Physician Postdoctoral Fellow. This work was supported by an NIH grant to E. W. and A. L.
PY - 1998/6/26
Y1 - 1998/6/26
N2 - 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.
AB - 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.
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U2 - 10.1016/S0092-8674(00)81461-0
DO - 10.1016/S0092-8674(00)81461-0
M3 - Article
C2 - 9657150
AN - SCOPUS:0032568802
SN - 0092-8674
VL - 93
SP - 1171
EP - 1182
JO - Cell
JF - Cell
IS - 7
ER -