Worm Breeder's Gazette 11(2): 105
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.
We reported previously the characterization of 7 dominant vulvaless ( Vul) mutations, isolated as dominant suppressors of a lin-16 multivulva (Muv) mutation [WBG 10 (3): 132]. These mutations, six of which are recessive lethal, were found to be alleles of let-60, previously identified by recessive lethal alleles [Clark et al., Genetics, 119: 345 (1988)]. We refer to these semi-dominant alleles as let-60(sd). The conclusions from our further studies on let-60 can be summarized as follows. let-60 and lin-34 are likely to be the same gene. let-60(sd) alleles were mapped between dpy-20 and the left break-point of nDf27. lin-34, identified only by semi-dominant Muv mutations, maps between dpy-20 and let-60 (G. Beitel, G. Jongeward, per. comms; our data). Our mapping data suggest that both are about 0.01 mu to the left of dpy-20. Also, lin-34 suppresses in trans the let-60(sd) Vul phenotype. In fact, we have isolated a lin-34(sd) allele as a dominant suppressor of the dominant suppressor phenotype of let-60(sd). More intriguingly, the lethality of some let-60(sd) homozygotes can be maternally rescued by lin-34/+.Vulvaless is a loss-of-function phenotype of let-60. We have isolated two intragenic revertants of let-60(sd) by reverting the dominant Vul or suppressor phenotype of let-60(sd). These revertants and the three previously isolated alleles (Baillie's lab) are likely null mutations because they behave similar to Dfs in heterozygotes. let-60(null)/let-60(sd) animals from a lin-34/let-60(sd) mother show a more severe defect in vulval induction (0%) than let-60(sd)/+ (57% for the allele used), indicating that Vul is a loss-of-function phenotype. Thus, because Df/+ has wildtype vulva, let-60(sd) alleles are dominant negative mutations. The level of let-60 activity controls VPCs fates. In let-60(sd)/+ animals, let-60 activity is lower than that in let-60(null)/+, resulting in a Vul phenotype. We propose, in light of our argument that lin-34(sd) are alleles of let-60, that a lin-34(sd) mutation results in elevation of let-60 activity and consequently a gonad signal independent Muv phenotype. Thus, a high level of let-60 activity specifies 1 or 2 while a low level specifies 3 . It is also conceivable that lin-34(sd) may be mutations in a distinct gene located very close to let-60, but nonetheless result in an increase of let-60 activity. Genetic interactions of let-60/lin-34 with other genes suggest its position in the vulval induction pathway. The following pathway was deduced from examination of double mutant phenotypes: [See Figure 1]