title: Activation of Wnt signaling bypasses the requirement for RTK/Ras signaling during C. elegans vulval induction.
abstract: During Caenorhabditis elegans vulval development, activation of receptor tyrosine kinase/Ras and Notch signaling pathways causes three vulval precursor cells (VPCs) to adopt induced cell fates. A Wnt signaling pathway also acts in cell fate specification by the VPCs, via regulation of the Hox gene lin-39. We show here that either mutation of pry-1 or expression of an activated BAR-1 beta-catenin protein causes an Overinduced phenotype, in which greater than three VPCs adopt induced cell fates. This indicates that pry-1, which encodes a C. elegans axin homolog, acts as a negative regulator of Wnt signaling in the VPCs. Loss of activity of the APC homolog apr-1 increases the penetrance of this Overinduced phenotype, suggesting that APR-1 may play a negative role in Wnt signaling in this process in C. elegans similar to APC proteins in other systems. The Overinduced phenotype is suppressed by reduction of function of the genes pop-1 TCF and lin-39 Hox. Surprisingly, the Overinduced phenotype caused by hyperactivated Wnt signaling is not dependent on signaling through the Ras pathway. These data suggest that hyperactivation of Wnt signaling is sufficient to cause VPCs to adopt induced fates and that a canonical Wnt pathway may play an important role during C. elegans vulval induction.
authors.affiliation: Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland 21250, USA.
authors.forename: Julie E
authors.initials: JE
authors.lastname: Gleason
authors.forename: Hendrik C
authors.initials: HC
authors.lastname: Korswagen
authors.forename: David M
authors.initials: DM
authors.lastname: Eisenmann
mesh_terms: D025601:Adenomatous Polyposis Coli Protein / Q000378:metabolism; D000818:Animals; D017173:Caenorhabditis elegans / Q000196:embryology* / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins; D002352:Carrier Proteins / Q000378:metabolism; D002450:Cell Communication; D003598:Cytoskeletal Proteins / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000502:physiology; D004627:Embryonic Induction / Q000502:physiology*; D005260:Female; D015870:Gene Expression; D011905:Genes, ras / Q000502:physiology*; D015801:Helminth Proteins / Q000502:physiology*; D006609:High Mobility Group Proteins / Q000502:physiology; D018398:Homeodomain Proteins / Q000502:physiology; D006358:Hot Temperature; D019476:Insect Proteins / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D009154:Mutation; D010641:Phenotype; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics*; D013489:Suppression, Genetic; D014844:Vulva / Q000166:cytology / Q000196:embryology*; D051153:Wnt Proteins; D029961:Zebrafish Proteins
chemical_list: D025601:Adenomatous Polyposis Coli Protein; D029742:Caenorhabditis elegans Proteins; D002352:Carrier Proteins; D003598:Cytoskeletal Proteins; D004268:DNA-Binding Proteins; D015801:Helminth Proteins; D006609:High Mobility Group Proteins; D018398:Homeodomain Proteins; D019476:Insect Proteins; D036341:Intercellular Signaling Peptides and Proteins; D011518:Proto-Oncogene Proteins; C117260:Pry-1 protein, C elegans; D051153:Wnt Proteins; D029961:Zebrafish Proteins; C115014:bar-1 protein, C elegans; C108673:lin-39 protein, C elegans; C096787:pop-1 protein, C elegans; C067715:APR-1 pheromone-binding protein, Antheraea pernyi