Worm Breeder's Gazette 10(2): 83

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.

Suppressors of a lin-12 Hypomorph

Meera Sundaram and Iva Greenwald

We have been reverting a hypomorphic lin-12 allele with the goal of 
identifying other genes which interact with lin-12 in the process of 
cell fate determination.  Since this allele has a lowered (but non-
null) level of lin-12 activity, the screen is primarily designed to 
detect loss of function mutations in negative effectors of lin-12, in 
contrast to screens involving reversion of lin-12(d) alleles (Ferguson 
et al, CSH Mtg., 1983; Thomas and Horvitz, CSH Mtg., 1987).
lin-12(n676n930) is an intragenic revertant of the mild lin-12(d) 
allele n676 and appears to be a hypomorph by several criteria: 1) the 
n930 mutation is tightly linked to the original n676 mutation; 2) the 
n930 mutation eliminates lin-12(d) activity in cis but not in trans; 3)
while most hermaphrodites have one anchor cell, some have two anchor 
cells like lin-12(0) animals, and the penetrance of this phenotype is 
enhanced in trans to a lin-12(0) allele; and 4) in dosage studies with 
a lin-12(d) allele, lin-12(n676n930) acts as though it has a level of 
lin-12 activity intermediate between that of wild type and lin-12(0).  
This allele is temperature sensitive, such that at 15 C mutant animals 
are phenotypically wild type (Egl+), while at 25 C they are 100% Egl-.  
Temperature shift experiments demonstrate that the temperature 
sensitive period is after the L2 stage, so the primary defect in these 
animals is probably not in the AC/VU decision, but may be in the vulva 
cells themselves.
After mutagenizing lin-12(n676n930) hermaphrodites with EMS and 
screening for eggs in the F2, we have isolated 17 independent 
extragenic dominant and recessive suppressors.  The recessive 
suppressors have no obvious dissecting microscope phenotype in a lin-
12(+) background, and define at least 3 different complementation 
groups: sup-25(e1948) and sup(ar22) map on linkage group V between dpy-
11 and unc-42, near the eT1 breakpoint, and sup(ar25) maps on the X 
chromosome between lon-2 and unc-58.  Initial characterization of sup-
25(e1948) has shown that 1) e1948 has no effect on the lin-12(0) 
allele n941; 2) e1948 does not appear to be allele, state, or tissue 
specific in that it increases the gain of function Egl- defect of lin-
12(d)/+, and at 15 C, the permissive temperature for lin-12(n676n930), a 
large percentage of lin-12(n676n930); e1948 hermaphrodites lack anchor 
cells like lin-12(d) hermaphrodites.
In light of the recently discovered homology between lin-12 and glp-
1 (John Yochem), we point out that none of these suppressors has a 
dumpy phenotype.  dpy-10(e128), which suppresses some ts glp-1 mutants 
(Eleanor Maine), and various other dpy markers checked during the 
course of mapping experiments do not suppress lin-12(n676n930).