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Mol. Cell. Biol., 02 1996, 529-537, Vol 16, No. 2
WS Katz, GM Lesa, D Yannoukakos, TR Clandinin, J Schlessinger and PW Sternberg
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.
Copyright © 1996, American Society for Microbiology
A point mutation in the extracellular domain activates LET-23, the Caenorhabditis elegans epidermal growth factor receptor homolog
Howard Hughes Medical Institute, California Institute of Technology, Pasadena, 91125, USA.
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