Abstract
Nicastrin is a recently identified member of high-molecular weight complexes containing presenilin. The Caenorhabditis elegans homolog of nicastrin, aph-2, was shown to be required for GLP-1/Notch signaling in the early embryo. In addition to the maternal-effect embryonic lethal phenotype, aph-2 mutant animals also display an egg-laying defect. We show that this latter defect is related to the SEL-12/presenilin egg-laying defect. We also show that aph-2 and sel-12 genetically interact and cooperate to regulate LIN-12/Notch signaling in the development of the somatic gonad. In addition, aph-2 and lin-12/Notch genetically interact. We illustrate a new role for aph-2 in facilitating lin-12 signaling in the somatic gonad, thus providing evidence that APH-2 is involved in both GLP-1/Notch- and LIN-12/Notch-mediated signaling events. Finally, we demonstrate that nicastrin can partially substitute for aph-2, suggesting a conservation of function between these proteins.
Original language | English (US) |
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Pages (from-to) | 654-661 |
Number of pages | 8 |
Journal | Developmental Biology |
Volume | 240 |
Issue number | 2 |
DOIs | |
State | Published - Dec 15 2001 |
Keywords
- APH-2
- Alzheimer's disease
- C. elegans
- LIN-12
- Nicastrin
- Notch
- Presenilin
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology