Worm Breeder's Gazette 12(2): 96 (January 1, 1992)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Alleles of the genes unc-101 and sli-1 (suppressor of lineage defect) were recovered as suppressors of the weak let-23 vulvaless (Vul) allele sy1 .Animals of genotype unc-101 ; let-23 ( sy1 )or let-23 ( sy1 ); sli-1 are often hyperinduced (Hin), displaying excess (greater than 3 VPCs) gonad-dependent vulval differentiation. However, animals bearing wild-type alleles of let-23 in combination with mutant alleles of either suppressor display no vulval induction defects. Certain sli-1 alleles in combination with any of the viable alleles of unc-101 display greater than wild-type induction (about 120%). Other alleles of sli-1 in combination with unc-101 do not display an obvious synthetic phenotype. The alleles that display the synthetic phenotype may be the stronger sli-1 alleles since they are the best suppressors of sy97 ,a slightly more severe subviable allele of let-230 .
This synthetic phenotype is not Hin. Residual (partially gonad-independent) vulval differentiation was observed in eight of nine animals in which the somatic gonad (+/- germ line) precursors were ablated in the L1 stage. This vulval differentiation averaged 62% (or approximately 2 VPCs induced per animal).
These two genes may encode partially redundant negative regulators of the let-23 signal transduction pathway. The wild-type function of these activities may be to lower the basal level of signal transduction. We are in the process of determining whether these genes interact with other genes that display a synthetic Muv phenotype, although neither lin-15 (A)nor lin-15 (B)is sufficient to suppress the Vul phenotype of let-23 ( sy1 ).