¹Centre for Cellular and Molecular Biology, Hyderabad, India

Correspondence: Dr PR Rao, Drosophila Genetics, Centre for Cellular and Molecular Biology, Uppal Road, Tarnaka, Hyderabad, Andhra Pradesh 500 007, India. E-mail: prashanth21676@gmail.com

Received 16 May 2007; Revised 4 September 2007; Accepted 1 October 2007; Published online 29 October 2007.

Abstract

There have been conflicting reports on the requirement of GSK-3-mediated phosphorylation of the tumor suppressor adenomatous polyposis coli (APC) vis-à-vis its ability to bind and degrade -catenin. Using a unique combination of loss of function for Shaggy/GSK-3 and a gain of function for human APC in Drosophila, we show that misexpressed human APC (hAPC) can still sequester Armadillo/-catenin. In addition, human APC could suppress gain of Wnt/Wingless phenotypes associated with loss of Shaggy/GSK-3 activity, suggesting that sequestered Armadillo/-catenin is non-functional. Based on these studies, we propose that binding per se of -catenin by APC does not require phosphorylation by GSK-3.