Work

LET-23 Receptor Localization by the Cell Junction Protein LIN-7 during C. elegans Vulval Induction

Year: 1996

Type: article

Abstract: 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.

Source: Cell

DOI: 10.1016/s0092-8674(00)81096-x

Authors: Jeffrey S Simske, Susan M Kaech, Stacey A Harp, Stuart K Kim

Institutions: Stanford Medicine, Stanford University

Language: English

Topic: Developmental Biology and Gene Regulation

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

Open Access status: hybrid

Estimated APC paid: $11,400

Funder: National Institute of General Medical Sciences