We have isolated more than 40 alleles of
sli-1 (suppressor of lineage defect) as silent suppressors of the Vulvaless (Vul) phenotype of weak alleles of
let-23. sli-l mutations suppress the Vul, Male Abnormal and Lethal phenotypes of non-null alleles of
let-23, but do not suppress the lethality of a null allele of
let-23. Since these mutations are silent and do not suppress nulls, we believe that sli-l is a negative regulator of
let-23, rather than a target of
let-23 activity. Certain sli-l and
let-23 alleles show allele-specific interactions, suggesting that these two gene products directly interact. Iet-23; sli-l double mutants are generally Hyperinduced (or Hin; more than three of the vulval precursor cells respond to the inductive signal in a gonad-dependent manner). Hin is believed to be a reduction-of-function phenotype of some of the Vul genes. sli-l suppresses both hypomorphic and null alleles of
lin-2 and
lin-7 to Hin. Since the sli-l allele used suppresses a strong hypomorphic
let-23 allele to wild-type, sli-l is not simply increasing the dosage of let- 23 or another component of the vulval induction pathway. sli-l suppresses weak alleles of
lin-3 but does not cause these animals to become Hin. sli-l does not suppress
let-60 or
lin-46, two genes acting after
let-23 in the vulval induction pathway. Therefore sli-l acts near
let-23 in the pathway. sli-l and
unc-101, another suppressor of the vulval defect of weak alleles of
let-23, show a synthetic vulval phenotype, such that
unc-101; sli-l double mutants can display as much as 130% induction, where 100% is wild-type induction. We believe that sli-l is a partially redundant negative regulator of
let-23 or some other early component of the vulval induction pathway.