A point mutation in the extracellular domain activates LET-23, the Caenorhabditis elegans epidermal growth factor receptor homolog.

Abstract:

:The let-23 gene encodes a Caenorhabditis elegans homolog of the epidermal growth factor receptor (EGFR) necessary for vulval development. We have characterized a mutation of let-23 that activates the receptor and downstream signal transduction, leading to excess vulval differentiation. This mutation alters a conserved cysteine residue in the extracellular domain and is the first such point mutation in the EGFR subfamily of tyrosine kinases. Mutation of a different cysteine in the same subdomain causes a strong loss-of-function phenotype, suggesting that cysteines in this region are important for function and nonequivalent. Vulval precursor cells can generate either of two subsets of vulval cells (distinct fates) in response to sa62 activity. The fates produced depended on the copy number of the mutation, suggesting that quantitative differences in receptor activity influence the decision between these two fates.

journal_name

Mol Cell Biol

authors

Katz WS,Lesa GM,Yannoukakos D,Clandinin TR,Schlessinger J,Sternberg PW

doi

10.1128/mcb.16.2.529

subject

Has Abstract

pub_date

1996-02-01 00:00:00

pages

529-37

issue

2

eissn

0270-7306

issn

1098-5549

journal_volume

16

pub_type

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