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.