Article

Presenilin-1 inhibits δ-catenin-induced cellular branching and promotes δ-catenin processing and turnover

The College of Pharmacy, Chonnam National University, Gwangju, Republic of Korea; Department of Anatomy and Cell Biology, The Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA; The Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, Republic of Korea
Biochemical and Biophysical Research Communications DOI:10.1016/j.bbrc.2006.10.135 pp.903-908

ABSTRACT Although δ-catenin/neural plakophilin-related armadillo protein (NPRAP) was reported to interact with presenilin-1 (PS-1), the effects of PS-1 on δ-catenin have not been established. In this study, we report that overexpression of PS-1 inhibits the δ-catenin-induced dendrite-like morphological changes in NIH 3T3 cells and promotes δ-catenin processing and turnover. The effects of PS-1 on endogenous δ-catenin processing were confirmed in hippocampal neurons overexpressing PS-1, as well as in the transgenic mice expressing the disease-causing mutant PS-1 (M146V). In addition, disease-causing mutant PS-1 (M146V and L286V) enhanced δ-catenin processing, whereas PS-1/γ-secretase inhibitors could block the formation of processed forms of δ-catenin. Together, our findings suggest that PS-1 can affect δ-catenin-induced morphogenesis possibly through the regulation of its processing and stability.

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Keywords

disease-causing mutant PS-1
 
endogenous δ-catenin processing
 
hippocampal neurons overexpressing PS-1
 
NIH 3T3 cells
 
NPRAP
 
promotes δ-catenin processing
 
PS-1
 
PS-1 inhibits
 
PS-1/γ-secretase inhibitors
 
transgenic mice
 
δ-catenin
 
δ-catenin processing
 
δ-catenin-induced dendrite-like morphological changes
 
δ-catenin-induced morphogenesis
 
δ-catenin/neural plakophilin-related armadillo protein
 

Jin-Sook Kim