In order to explore the role of
lin-2,
lin-7 and
lin-10 in LET-23 receptor signaling in vulval induction, we have identified mutations that suppress the vulvaless phenotype of
lin-10(
n1390). The
lin-10(
n1390) mutation causes 99.7% of animals to exhibit a vulvaless phenotype. We have identified 29 suv mutations that suppress the
lin-10 vulvaless phenotype; specifically, less than 10% of
lin-10(
n1390); suv animals are vulvaless. Twenty-seven of these mutations have been characterized and fall into three complementation groups:
suv-1 (10 alleles),
suv-2 (13 alleles) and
suv-3 (4 alleles). We have begun to genetically analyze the suv genes. First, to address the role of suv genes in the repression of vulval induction, we observed animals that had a single mutation in either
suv-1,
suv-2 or
suv-3. Each of the single mutants showed wild-type vulval induction, indicating that these suv genes are not individually essential for repression of vulval induction. Second, we addressed whether these suv genes genetically interact with genes in the RTK signaling pathway (
lin-2 EGF,
let-23 receptor and
let-60 ras) or with genes involved in LET-23 receptor localization (
lin-2 MAGUK and
lin-7 PDZ). We found that
suv-1 mutations suppress the vulvaless defect associated with mutations in both classes. In contrast,
suv-2 mutations only suppressed the vulvaless phenotype associated with mutations in genes of the second class (
lin-2 ,
lin-7 and
lin-10). We therefore speculate that
suv-2 may interact more closely with
lin-2,
lin-7 or
lin-10 than with genes that act directly in the RTK signaling pathway. One possible role for
suv-2 is that it might be involved in apical localization of the LET-23 receptor in
lin-2,
lin-7 or
lin-10 mutants. Mutations in
lin-2 and
lin-7 cause delocalization of LET-23 receptor to the apical side of vulval precursor cells and result in a vulvaless phenotype. Mutations in
suv-2 could rescue the vulvaless defect of
lin-2 and
lin-7 by restoring LET-23 to the basolateral membrane compartment of P6.p. Another possible role for
suv-2 is that it might normally limit the amount of LET-23 in P6.p so that
suv-2 mutations would result in increased LET-23 levels. Overexpression of LET-23 suppresses the vulvaless phenotype of mislocalization mutants, and
suv-2 mutations might also suppress the vulvaless phenotype in these mutants by increasing the amount of LET-23.
suv-2 and
suv-3 have both been mapped to the
dpy-6-
unc-9 interval of chromosome X and are currently being molecularly cloned.