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Mutations in the Caenorhabditis elegans let-23 EGFR-like gene define elements important for cell-type specificity and function

Aroian, Raffi V. and Lesa, Giovanni M. and Sternberg, Paul W. (1994) Mutations in the Caenorhabditis elegans let-23 EGFR-like gene define elements important for cell-type specificity and function. EMBO Journal, 13 (2). pp. 360-366. ISSN 0261-4189. PMCID PMC394816. https://resolver.caltech.edu/CaltechAUTHORS:20190515-111211560

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Abstract

The Caenorhabditis elegans let-23 gene is a genetically characterized member of the epidermal growth factor receptor (EGFR) tyrosine kinase family. Mutations in let-23 can produce five phenotypes in the nematode. Alleles of let-23 include null alleles, reduction-of-function alleles and alleles that disrupt function in some cell types and not others. We have sequenced some of these mutations to identify sequences and regions important for overall let-23 function and for let-23 function in specific cell types. Our data indicate that in vivo, the receptor's C-terminus can be partitioned into at least three domains that each contribute to receptor function in different cell types. In particular, we find distinct domains that mediate hermaphrodite fertility and vulval induction. Our data also demonstrate for the first time that a single, conserved residue in the ligand binding domain is critical for function in vivo and that mutations in the extracellular cysteines characteristic of the EGFR family can lead to a partial or a complete reduction of receptor function.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC394816PubMed CentralArticle
ORCID:
AuthorORCID
Sternberg, Paul W.0000-0002-7699-0173
Additional Information:© 1994 European Molecular Biology Organization. Received on September 1, 1993. We thank Makota Koga for unpublished let-23 genomic sequence. We also thank Pantelis Tsoulfas, Wendy Fantl, André Brändli, Helen Chamberlin, Andy Golden, Becky Kellum, Bin Liu, Michelle Moritz, Naomi Robinson, Tim Steams and Yixian Zheng for critical reading of this manuscript. G.M.L. was supported by a Merck pre-doctoral fellowship. This research was supported by USPHS grant HD23690 to P.W.S. P.W.S. is an investigator of the Howard Hughes Medical Institute.
Funders:
Funding AgencyGrant Number
MerckUNSPECIFIED
NIHHD23690
Howard Hughes Medical Institute (HHMI)UNSPECIFIED
Issue or Number:2
PubMed Central ID:PMC394816
Record Number:CaltechAUTHORS:20190515-111211560
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20190515-111211560
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:95512
Collection:CaltechAUTHORS
Deposited By: Tony Diaz
Deposited On:16 May 2019 02:42
Last Modified:03 Oct 2019 21:14

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