The SEL-12 presenilin mediates induction of the Caenorhabditis elegans uterine π cell fate
The SEL-12 presenilin mediates induction of the Caenorhabditis elegans uterine π cell fate
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DOI:
10.1006/dbio.2001.0374
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发表时间:
2001-09-01
影响因子:
2.7
通讯作者:
Newman, AP
中科院分区:
文献类型:
--
作者:
Cinar, HN;Sweet, KL;Newman, AP
During Caenorhabditis elegans hermaphrodite development, the anchor cell induces the vulva and the uterine a cells whose daughters connect to the vulva, thereby organizing the uterine-vulval connection. Both the initial selection of a single anchor cell during the anchor cell vs. ventral uterine precursor 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 gene family can cause early onset Alzheimer's disease when mutated and are also required for LIN-12/Notch signaling during development. We have shown that, in C. elegans, mutation of the sel-12-encoded presenilin results in pi cell induction defects. By contrast, other lin-12-mediated cell fate decisions occur normally in sel-12 mutants due to the redundant function of a second 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 cells. sel-12-mediated pi cell fate specification provides a useful system for the analysis of presenilin function at single cell resolution. (C) 2001 Academic Press.