Extragenic suppressors of a dominant masculinizing her-1 mutation in C. elegans identify two new genes that affect sex determination in different ways.
Summary: The her-1 regulatory switch gene in C. elegans sex determination is normally active in XO animals, resulting in male development, and inactive in XX animals, allowing hermaphrodite development. The her-1(n695gf) mutation results in the incomplete transformation of XX animals into phenotypic males. We describe four extragenic mutations that suppress the masculinized phenotype of her-1(n695gf) XX. They define two previously undescribed genes, sup-26 and sup-27. All four mutations exhibit semidominance of suppression and by themselves have no visible effects on sex determination in otherwise genotypically wild-type XX or XO animals. Analysis of interactions with mutations in the major sex-determining genes show that sup-26 and sup-27 influence sex determination in fundamentally different ways. sup-26 appears to act independently of her-1 to negatively modulate synthesis or function of tra-2 in both XX and XO animals. sup-27 may play a role in X-chromosome dosage compensation and influence sex determination indirectly.[1]References
- Extragenic suppressors of a dominant masculinizing her-1 mutation in C. elegans identify two new genes that affect sex determination in different ways. Manser, J., Wood, W.B., Perry, M.D. Genesis (2002) [Pubmed]
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