Worm Breeder's Gazette 10(1): 124
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.
n695 is a semi-dominant allele of her-1 which partially masculinizes XX animals. In an n695 homozygous strain, 100% of the XX hermaphrodites are egg-laying defective (Egl). A smaller subset of these animals are further masculinized and exhibit a partial transformation of the tail towards a more male fate (Tra) (Carol Trent, personal communication). These weak masculinizing effects of n695 are sensitive to small perturbations in the rest of the sex determination pathway. For example, n695 in combination with weak alleles of tra-2 masculinizes XX animals much more than either single mutation alone. In addition, duplications of X which have no phenotype in a her-1(+) background can suppress the masculinization caused by n695 (Anne Villeneuve, personal communication). Using the phenotype of n695 as an assay, we are attempting to identify regions of the X chromosome which interact with the sex determination pathway in a dose-dependent fashion by looking for X- linked deficiencies which increase the masculinization caused by n695. These deficiencies could interact with the rest of the sex determination pathway by removing a region of X that is important in the assessment of the X/A ratio. As a consequence, the apparent X/A ratio would be reduced and the animal would be directed toward a more male developmental fate. Alternatively, they might uncover a haplo insufficient gene that is required for hermaphrodite development in n695 XX animals, thus revealing a function that is likely to be important for proper sex determination in wild-type animals. Thus far, the n695-deficiency assay has localized several regions of the X chromosome, which when present in one copy, cause n695 XX animals to be highly masculinized. One masculinizing region, defined by the deficiency uDf1, results in the production of some n695 XX males which are able to mate. This deficiency, uDf1, has been shown by L. Miller to uncover the gene xol-1. This result is in agreement with the previous finding that some n695; xol-1(y9)/+ XX animals are transformed into males capable of mating (L. Miller, personal communication). Other masculinizing regions have been identified on the right arm of X. We have looked at the nested set of deficiencies on the right arm of X and have found that a subset of these also have a dominant masculinizing effect when placed in combination with n695 (Table 1, Figure 1). In one copy, these deficiencies increase the number of transformed animals. These deficiencies define two small regions which when present in one copy appear to result in further masculinization of n695 XX animals. [See Figure 1] [See Figure 2]