The SEL-12 presenilin mediates induction of the Caenorhabditis elegans uterine pi cell fate

During Caenorhabditis elegans hermaphrodite development, the anchor cell in duces the vulva and the uterine a cells whose daughters connect to the vulv a, thereby organizing the uterine-vulval connection. Both the initial selec tion of a single anchor cell during the anchor cell vs. ventral uterine pre cursor cell decision and the subsequent induction of the a cell fate by the anchor cell are mediated by the lin-12 gene. Members of the presenilin gen e family can cause early onset Alzheimer's disease when mutated and are als o required for LIN-12/Notch signaling during development. We have shown tha t, in C. elegans, mutation of the sel-12-encoded presenilin results in pi c ell induction defects. By contrast, other lin-12-mediated cell fate decisio ns occur normally in sel-12 mutants due to the redundant function of a seco nd C. elegans presenilin called HOP-1. We found that the sel-12 egg-laying defect was partially rescued by expression of the sel-12 gene in the pi cel ls. sel-12-mediated pi cell fate specification provides a useful system for the analysis of presenilin function at single cell resolution. (C) 2001 Ac ademic Press.