Worm Breeder's Gazette 10(3): 133
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.
To find additional genes involved in vulval development and to identify mutations that elevate the inductive signal, we are screening for suppressors of the egg-laying defective (Egl-) phenotype of a non- null non-amber let-23 allele, sy1. Only 93% of hermaphrodites homozygous for sy1 are Egl- and therefore sy1 cannot be reverted. To circumvent this problem we have taken advantage of the observation that sy1/Df strains are completely penetrant for the Egl phenotype ( 0/3500 worms laid eggs). In our first screen, one suppressor, sy90, was isolated as a suppressor of the Egl- phenotype of a strain of the let-238(mn229) 1) + mnDf61In subsequent mutageneses, loss of the balancer, let-238, became a problem. To address this problem, we constructed let-238(mn229) 1) + sqt-1(e1350) + mnDf67 unc-4(e120) + In this strain, recombination between let-23 and let-23+ should be minimal since let-238 is one of the two genes nearest the left end of mnDf67, and e1350 acts as a dominant marker of heterozygosity. Using this strain, we have screened 17,000 mutagenized haploid genomes and have isolated several Egl+ strains. The first suppressor, sy90, is an extragenic semidominant suppressor of homozygous sy1 with no obvious phenotype in a let-23(+) background. sy90 also suppresses let-23( n1045) from 2% Egl+ to 34% Egl+ at 15 C. However, sy90 does not suppress the lethality of let-23(mn23), an allele that is lethal when homozygous and fails to complement the vulval defect of sy1. We have tentatively mapped sy90 to chromosome IV based on loose linkage to dpy- 20(e1282). sy90 acts as if it increases let-23 vulval activity in a dose-dependent manner. [See Figure 1]