Worm Breeder's Gazette 10(2): 24
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.
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.