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.

A Screen for Suppressors of the Vulvaless Phenotype of let-23(sy1)

Gregg Jongeward and Paul Sternberg

Figure 1

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 
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]

Figure 1