sli-1 is a negative regulator of the vulval induction pathway in C. elegans. Reduction-of-function mutations in
let-23 ,a C. elegans homolog of the mammalian EGF receptor, cause a vulvaless (Vul) phenotype. While mutations in
sli-1 alone are silent (i.e., wild-type vulva),
let-23 ;
sli-1 double mutants display a greater responsiveness to the inductive signal, either having a hyperinduced vulval phenotype (Hin) or a less severe Vul phenotype. Thus, the wild-type function of
sli-1 appears to be the negative regulation of vulval induction; a
sli-1 mutation increases the number of cells forming vulval tissue. We have rescued the
sli-1 mutant phenotype by microinjection with the cosmid T18D5 . [See Figure] Genetic mapping showed that
sli-1 lies between
egl-17 and
unc-1 .The RFLP
stP41 was mapped near and to the left of
unc-1 (Anne Villeneuve, pers. comm.). We assumed that
stP41 was near
unc-1 ,that the contig extended to the left end of chromosome X, and that
egl-17 was located at the end of the chromosome. We therefore chose the centrally located cosmids F02G3 ,T18D5 ,F25H6 ,F25E2 .These cosmids were injected individually into
let-23 (
sy1);
sli-1 (
sy143)double mutants along with
rol-6 DNA as a transgenic marker, and stable transgenic lines were recovered and scored. Microinjection of the cosmid T18D5 rescued the Hin phenotype of the
let-23 ;
sli-1 parental strain and yielded transgenic progeny with the Vul phenotype typical of a
let-23 mutation. Cosmids F02G3 ,F25H6 ,and F25E2 failed to rescue the Hin phenotype in transgenic animals. An additional allele of
sli-1 ,
sy129 ,was also rescued by the cosmid T18D5 in
let-23 (
sy1);
sli-1 (
sy129)double mutants. [See Figure]