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Nat Cell Biol. 2002 Mar;4(3):208-13.

A Drosophila APC tumour suppressor homologue functions in cellular adhesion.

Author information

1
MRC Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, UK.

Abstract

Adenomatous polyposis coli (APC) is an important tumour suppressor in the intestinal epithelium. Its function in reducing nuclear beta-catenin and T-cell factor (TCF)-mediated transcription is conserved from Drosophila to mammals. But APC proteins are also associated with the plasma membrane. Here, we show that mutational inactivation of Drosophila E-APC causes delocalization of Armadillo (the Drosophila beta-catenin) but not DE-cadherin from adhesive plasma membranes. Extensive gaps between these membranes are visible at the ultrastructural level. The oocyte is also mislocalized in E-APC mutant egg chambers, a phenotype that results from a failure of cadherin-based adhesion. These results indicate that Drosophila APC functions in cellular adhesion; these results could have implications for colorectal adenoma formation and tumour progression in humans.

PMID:
11862214
DOI:
10.1038/ncb755
[Indexed for MEDLINE]

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