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Evidence for functional and physical association between Caenorhabditis elegans SEL-10, a Cdc4p-related protein, and
G Wu1, E J Hubbard, J K Kitajewski
1Department of Pathology and Center for Reproductive Sciences, Howard Hughes Medical Institute, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Abstract:
Mutations in either of two human presenilin genes (PS1 and PS2) cause Alzheimer's disease. Here we describe genetic and physical interactions between Caenorhabditis elegans SEL-10, a member of the Cdc4p family of proteins, and SEL-12, a C. elegans presenilin. We show that loss of sel-10 activity can suppress the egg-laying defective phenotype associated with reducing sel-12 activity, and that SEL-10 can physically complex with SEL-12. Proteins of the Cdc4p family have been shown to target proteins for ubiquitin-mediated turnover. The functional and physical interaction between sel-10 and sel-12 therefore offers an approach to understanding how presenilin levels are normally regulated.