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.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Levitan D,Yu G,St George Hyslop P,Goutte Cdoi
10.1006/dbio.2001.0486subject
Has Abstractpub_date
2001-12-15 00:00:00pages
654-61issue
2eissn
0012-1606issn
1095-564Xpii
S0012160601904865journal_volume
240pub_type
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journal_title:Developmental biology
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journal_title:Developmental biology
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