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
Newman, AP
中科院分区:
生物学3区
文献类型:
--
作者:
Cinar, HN;Sweet, KL;Newman, AP

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在秀丽隐杆线虫两性发育过程中,锚定细胞诱导外阴和子宫腺细胞与外阴相连,从而组织子宫-外阴连接。在锚定细胞对腹侧子宫前体细胞的决定过程中,单个锚定细胞的初始选择和随后锚定细胞对a细胞命运的诱导都是由Lin-12基因介导的。早老素基因家族的成员在突变时会导致早发性阿尔茨海默病,并且在发育过程中也是Lin-12/Notch信号所必需的。我们已经证明,在线虫中,SEL-12编码的早老素突变会导致圆周率细胞诱导缺陷。相比之下,其他由Lin-12介导的细胞命运决定通常发生在sel-12突变体中,这是由于第二个线虫早老素HOP-1的冗余功能。我们发现,在pi细胞中表达sel-12基因可以部分挽救sel-12的产卵缺陷。SEL-12介导的pI细胞命运调控为在单细胞分辨率下分析早老素功能提供了一个有用的系统。(C)2001年学术出版社。
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.