title: Suppressors of a lin-12 hypomorph define genes that interact with both lin-12 and glp-1 in Caenorhabditis elegans.
abstract: The lin-12 gene of Caenorhabditis elegans is thought to encode a receptor which mediates cell-cell interactions required to specify certain cell fates. Reversion of the egg-laying defective phenotype caused by a hypomorphic lin-12 allele identified rare extragenic suppressor mutations in five genes, sel-1, sel-9, sel-10, sel-11 and sel(ar40) (sel = suppressor and/or enhancer of lin-12). Mutations in each of these sel genes suppress defects associated with reduced lin-12 activity, and enhance at least one defect associated with elevated lin-12 activity. None of the sel mutations cause any obvious phenotype in a wild-type background. Gene dosage experiments suggest that sel-1 and sel(ar40) mutations are reduction-of-function mutations, while sel-9 and sel-11 mutations are gain-of-function mutations. sel-1, sel-9, sel-11 and sel(ar40) mutations do not suppress amorphic lin-12 alleles, while sel-10 mutations are able to bypass partially the requirement for lin-12 activity in at least one cell fate decision. sel-1, sel-9, sel-10, sel-11 and sel(ar40) mutations are also able to suppress the maternal-effect lethality caused by a partial loss-of-function allele of glp-1, a gene that is both structurally and functionally related to lin-12. These sel genes may therefore function in both lin-12 and glp-1 mediated cell fate decisions.
authors.affiliation: Department of Molecular Biology, Princeton University, New Jersey 08544.
authors.forename: M
authors.initials: M
authors.lastname: Sundaram
authors.forename: I
authors.initials: I
authors.lastname: Greenwald
mesh_terms: D000483:Alleles; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development / Q000502:physiology; D002450:Cell Communication / Q000235:genetics; D002874:Chromosome Mapping; D012734:Disorders of Sex Development / Q000235:genetics; D005260:Female; D017238:Genes, Helminth; D008297:Male; D009154:Mutation; D010058:Oviposition / Q000235:genetics; D010641:Phenotype; D013489:Suppression, Genetic; D014844:Vulva / Q000002:abnormalities / Q000254:growth & development