Sex determination in the nematode C. elegans: analysis of tra-3 suppressors and characterization of fem genes.
Mutations of the gene tra-3 result in partial masculinization of XX animals of C. elegans, which are normally hermaphrodites (males are XO). A total of 43 tra-3 revertants (one intragenic, 42 extragenic) have been isolated and analyzed, in the hope of identifying new sex-determination loci. Most (38) of the extra-genic suppressors cause partial or complete feminization of XX and XO animals; the remaining four are weak suppressors. The feminizing suppressors are mostly alleles of known sex-determining genes: tra-1 (11 dominant alleles), tra-2 (one dominant allele), fem-1 (four alleles) and fem-2 (four alleles), but 18 are alleles of a new gene, fem-3. Additional alleles have been isolated for the fem-2 and fem-3 genes, as well as fem-3 deficiencies. Mutations in fem-3 resemble alleles of fem-1 (previously characterized): putative null alleles result in complete feminization of XX and XO animals, transforming them into fertile females. Severe alleles of fem-2 also cause complete feminization of XX animals at all temperatures, but feminization of fem-2 XO animals is temperature-sensitive: complete at 25 degrees, incomplete at 20 degrees. As with fem-1, severe mutations of fem-2 and fem-3 are wholly epistatic to masculinizing alleles of tra-2 and tra-3, and epistatic to tra-1 masculinizing alleles in the germline, but not in the soma. All three fem genes are essential for male development and appear to have a dual role in promoting spermatogenesis and repressing tra-1 activity. All three fem genes exhibit strong maternal effects; the maternal contribution of fem gene products may be inactivated in XX animals by a posttranscriptional mechanism. Maternal contributions of wild-type fem-3 product are necessary for normal XO male development and XX hermaphrodite (as opposed to female) development.[1]References
- Sex determination in the nematode C. elegans: analysis of tra-3 suppressors and characterization of fem genes. Hodgkin, J. Genetics (1986) [Pubmed]
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