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

Katz, Wendy S. and Lesa, Giovanni M. and Yannoukakos, Drakoulis and Clandinin, Thomas R. and Schlessinger, Joseph and Sternberg, Paul W. (1996) A point mutation in the extracellular domain activates LET-23, the Caenorhabditis elegans epidermal growth factor receptor homolog. Molecular and Cellular Biology, 16 (2). pp. 529-537. ISSN 0270-7306. http://resolver.caltech.edu/CaltechAUTHORS:KATmcb96

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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.


Item Type:Article
Additional Information:Copyright © 1996, American Society for Microbiology Received 10 May 1995/Returned for modification 27 September 1995/Accepted 7 November 1995 We are grateful to Jim Thomas for providing sa62. We thank Giuseppe Tocchini-Valentini for providing an in vitro mutagenesis protocol, Lily Jiang and Katharine Liu for help in scoring sa62 phenotypes, and Raffi Aroian for many suggestions and stimulating discussions. Some strains were provided by the Caenorhabditis Genetics Center. This work was supported by a grant to P.W.S. from USPHS and by the HHMI, of which P.W.S. is an investigator and W.S.K. is an associate. G.M.L. is a Merck Graduate Fellow. T.R.C. was supported by an Amgen Fund fellowship.
Record Number:CaltechAUTHORS:KATmcb96
Persistent URL:http://resolver.caltech.edu/CaltechAUTHORS:KATmcb96
Alternative URL:http://mcb.asm.org/cgi/content/abstract/16/2/529
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ID Code:3413
Collection:CaltechAUTHORS
Deposited By: Archive Administrator
Deposited On:06 Jun 2006
Last Modified:26 Dec 2012 08:54

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