Worm Breeder's Gazette 10(2): 24

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y52 V, A Mutation in a New Gene, Masculinizes XX Animals

Leslie DeLong and Barbara Meyer

Figure 1

y52 was isolated as an apparent suppressor of the XO-specific 
lethality of xol-1(y9) (Miller et al.  WBG 10 #1).  Using the 
appropriate genetic markers we have shown that y52 does not rescue X0 
animals, but rather that it masculinizes XX animals.  XX animals 
homozygous for y52 exhibit a range of phenotypes from Egl 
hermaphrodite to pseudomale.  The most strongly transformed animals 
have a normal male body and gonad but stunted rays in the tail.  
Complete transformation to a mating XX male can occur if the animal is 
also homozygous for a mutation in xol-1.  The mutant phenotype of y52 
is more severe at 16 C (99.7% of animals have masculinized tails) than 
at 20 C (83% of animals have masculinized tails).  The mutation maps 
between unc-61 and unc-76 on V.
Epistasis tests place y52 upstream of her-1 on the sex determination 
pathway.  The strain unc-42 20) 
uces only hermaphrodite progeny, there is no 
detectable masculinization.  unc-42 20) 
animals also show no evidence of 
masculinization, supporting the interpretation that y52 acts upstream 
of her-1.  These epistasis results predict that fem-3(e1996) should be 
epistatic to y52, which we have demonstrated to be the case.
[See Figure 1]
We tested for altered X-linked gene expression in y52 animals using 
the lin-14 assay and found that there was no detectable effect.  The 
progeny of y52/+; lin-14(n179) hermaphrodites were examined; y52/y52 
animals were indistinguishable from their y52/+ and +/+ siblings and 
from lin-14(n179) control animals.  This result is consistent with the 
finding that y52 does not rescue the XO specific lethality of in xol-1(
y9).  Thus, y52 appears to be a mutation in a new tra gene.  We are 
screening for additional alleles of this gene to determine if our 
hypothesis is correct.
A new chauvinistic dpy mutation dpy-29, has been mapped to the same 
interval as y52 (Plenefish et al.  this issue).  dpy-29(y100) and y52 
complement fully for dumpiness, lethality, xol-1 suppression and XX 
masculinization, making it unlikely that these mutations are allelic.  
We are ordering dpy-29(y100) and y52 with respect to each other.

Figure 1