LET-23 receptor localization by the cell junction protein LIN-7 during C. elegans vulval induction.
In C. elegans, the anchor cell signal induces Pn.p cells to form the vulva by activating a conserved receptor tyrosine kinase pathway. lin-2 and lin-7 mutants exhibit a vulvaless phenotype similar to the phenotype observed when this signaling pathway is defective. We have found that LIN-7 is a cell junction-associated ... protein that binds to the LET-23 receptor tyrosine kinase. LET-23 is also localized to the cell junctions, and both LIN-2 and LIN-7 are required for this localization. LET-23 overexpression rescues the lin-2 or lin-7 vulvaless phenotype, suggesting that increased receptor density can compensate for mislocalization. These results suggest that proper localization of LET-23 receptor to the Pn.p cell junctions is required for signaling activity.
Mesh Terms:
Animals, Base Sequence, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cloning, Molecular, Embryonic Induction, Epithelium, Female, Genes, Helminth, Helminth Proteins, Intercellular Junctions, Membrane Proteins, Molecular Sequence Data, Mutation, Phenotype, Protein Structure, Tertiary, Proteins, Receptor, Epidermal Growth Factor, Sequence Homology, Amino Acid, Signal Transduction, Vulva
Animals, Base Sequence, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cloning, Molecular, Embryonic Induction, Epithelium, Female, Genes, Helminth, Helminth Proteins, Intercellular Junctions, Membrane Proteins, Molecular Sequence Data, Mutation, Phenotype, Protein Structure, Tertiary, Proteins, Receptor, Epidermal Growth Factor, Sequence Homology, Amino Acid, Signal Transduction, Vulva
Cell
Date: Apr. 19, 1996
PubMed ID: 8612272
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