Unknown

Dataset Information

0

Reverse genetic analysis of Caenorhabditis elegans presenilins reveals redundant but unequal roles for sel-12 and hop-1 in Notch-pathway signaling.


ABSTRACT: Mutations in the human presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease. Studies in Caenorhabditis elegans and in mice indicate that one function of presenilin genes is to facilitate Notch-pathway signaling. Notably, mutations in the C. elegans presenilin gene sel-12 reduce signaling through an activated version of the Notch receptor LIN-12. To investigate the function of a second C. elegans presenilin gene hop-1 and to examine possible genetic interactions between hop-1 and sel-12, we used a reverse genetic strategy to isolate deletion alleles of both loci. Animals bearing both hop-1 and sel-12 deletions displayed new phenotypes not observed in animals bearing either single deletion. These new phenotypes-germ-line proliferation defects, maternal-effect embryonic lethality, and somatic gonad defects-resemble those resulting from a reduction in signaling through the C. elegans Notch receptors GLP-1 and LIN-12. Thus SEL-12 and HOP-1 appear to function redundantly in promoting Notch-pathway signaling. Phenotypic analyses of hop-1 and sel-12 single and double mutant animals suggest that sel-12 provides more presenilin function than does hop-1.

SUBMITTER: Westlund B 

PROVIDER: S-EPMC26813 | biostudies-literature | 1999 Mar

REPOSITORIES: biostudies-literature

altmetric image

Publications

Reverse genetic analysis of Caenorhabditis elegans presenilins reveals redundant but unequal roles for sel-12 and hop-1 in Notch-pathway signaling.

Westlund B B   Parry D D   Clover R R   Basson M M   Johnson C D CD  

Proceedings of the National Academy of Sciences of the United States of America 19990301 5


Mutations in the human presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease. Studies in Caenorhabditis elegans and in mice indicate that one function of presenilin genes is to facilitate Notch-pathway signaling. Notably, mutations in the C. elegans presenilin gene sel-12 reduce signaling through an activated version of the Notch receptor LIN-12. To investigate the function of a second C. elegans presenilin gene hop-1 and to examine possible genetic interactions between hop-1 and se  ...[more]

Similar Datasets

| S-EPMC23751 | biostudies-literature
| S-EPMC16638 | biostudies-literature
| S-EPMC1460874 | biostudies-other
| S-EPMC2504490 | biostudies-literature
| S-EPMC6071610 | biostudies-other
| S-EPMC187465 | biostudies-literature
| S-EPMC5788535 | biostudies-literature
| S-EPMC316751 | biostudies-literature
| S-EPMC131058 | biostudies-literature
| S-EPMC2678165 | biostudies-literature