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APH-1 is a multipass membrane protein essential for the Notch signaling pathway in Caenorhabditis elegans embryos.

ABSTRACT: Early embryonic cells in Caenorhabditis elegans embryos interact through a signaling pathway closely related to the Notch signaling pathway in Drosophila and vertebrates. Components of this pathway include a ligand, receptor, the presenilin proteins, and a novel protein, APH-2, that is related to the Nicastrin protein in humans. Here we identify the aph-1 gene as a new component of the Notch pathway in Caenorhabditis elegans. aph-1 is predicted to encode a novel, highly conserved multipass membrane protein. We show that aph-1 and the presenilin genes share a similar function in that they are both required for proper cell-surface localization of APH-2/Nicastrin.

SUBMITTER: Goutte C

PROVIDER: S-EPMC117381 | biostudies-literature | 2002 Jan

REPOSITORIES: biostudies-literature

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APH-1 is a multipass membrane protein essential for the Notch signaling pathway in Caenorhabditis elegans embryos.

Goutte Caroline C Tsunozaki Makoto M Hale Valerie A VA Priess James R JR

Proceedings of the National Academy of Sciences of the United States of America 20020115 2

Early embryonic cells in Caenorhabditis elegans embryos interact through a signaling pathway closely related to the Notch signaling pathway in Drosophila and vertebrates. Components of this pathway include a ligand, receptor, the presenilin proteins, and a novel protein, APH-2, that is related to the Nicastrin protein in humans. Here we identify the aph-1 gene as a new component of the Notch pathway in Caenorhabditis elegans. aph-1 is predicted to encode a novel, highly conserved multipass membr ...[more]

PMID: 11792846

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Polycomb and Notch signaling regulate cell proliferation potential during <i>Caenorhabditis elegans</i> life cycle.

Project description:Stable cell fate is an essential feature for multicellular organisms in which individual cells achieve specialized functions. Caenorhabditis elegans is a great model to analyze the determinants of cell fate stability because of its invariant lineage. We present a tractable cell fate challenge system that uses the induction of fate-specifying transcription factors. We show that wild-type differentiated animals are highly resistant to fate challenge. Removal of heterochromatin marks showed marked differences: the absence of histone 3 lysine 9 methylation (H3K9) has no effect on fate stability, whereas Polycomb homolog mes-2 mutants lacking H3K27 methylation terminally arrest larval development upon fate challenge. Unexpectedly, the arrest correlated with widespread cell proliferation rather than transdifferentiation. Using a candidate RNAi larval arrest-rescue screen, we show that the LIN-12Notch pathway is essential for hyperplasia induction. Moreover, Notch signaling appears downstream of food-sensing pathways, as dauers and first larval stage diapause animals are resistant to fate challenge. Our results demonstrate an equilibrium between proliferation and differentiation regulated by Polycomb and Notch signaling in the soma during the nematode life cycle.

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