PMID:11862214

Citation	Hamada, F and Bienz, M (2002) A Drosophila APC tumour suppressor homologue functions in cellular adhesion. Nat. Cell Biol. 4:208-13
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.
Links	PubMed Online version:10.1038/ncb755
Keywords	Adenomatous Polyposis Coli/etiology; Adenomatous Polyposis Coli/genetics; Adenomatous Polyposis Coli Protein/genetics; Adenomatous Polyposis Coli Protein/physiology; Amino Acid Sequence; Animals; Armadillo Domain Proteins; Cadherins/metabolism; Cell Adhesion/genetics; Drosophila/cytology; Drosophila/embryology; Drosophila/genetics; Drosophila/metabolism; Drosophila Proteins/genetics; Drosophila Proteins/physiology; Female; Genes, APC; Genes, Insect; Humans; Insect Proteins/metabolism; Molecular Sequence Data; Oocytes/cytology; Phenotype; Point Mutation; Sequence Homology, Amino Acid; Trans-Activators; Transcription Factors
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