Abstract
Sex-lethal (Sxl) is a vital, X-chromosome gene involved in Drosophila sex determination. The most striking aspect of the phenotype of daughterless (da), an autosomal maternal-effect mutation, may be explained by effects on the functioning of the Sxl gene in the zygote. In this paper, new aspects of interactions between various combinations of Sxl and da alleles are explored in order to understand better the complex da phenotype. The study focuses on the relationship between maternal and zygotic da+ gene functions, and on the relationship between aspects of the da phenotype that are sex-specific and aspects that are not. The SxlM#1 allele, which counteracts the female-specific maternal effect of da, is shown to have no effect on two other aspects of the da phenotype (one maternal, one primarily zygotic) that are not sex-specific. The female-lethal da maternal effect is shown to kill daughters even when the progeny are entirely wild-type with respect to da. Recessive mutant alleles of the two genes can interact synergistically when both are heterozygous with their wild-type alleles, disrupting the development of most of the daughters. Surprisingly, even a deficiency of the da+ locus can produce a dominant, temperature-sensitive, female-lethal maternal effect. A new class of subliminal Sxlf alleles is described. These spontaneous mutations can confuse analysis of both da and Sxl if their presence is not appreciated. Finally, conditions are described that facilitate the study of the Enhancer of daughterless mutation.
Full Text
The Full Text of this article is available as a PDF (1.6 MB).
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- Bakken A. H. A cytological and genetic study of oogenesis in Drosophila melanogaster. Dev Biol. 1973 Jul;33(1):100–122. doi: 10.1016/0012-1606(73)90167-x. [DOI] [PubMed] [Google Scholar]
- Gans M., Audit C., Masson M. Isolation and characterization of sex-linked female-sterile mutants in Drosophila melanogaster. Genetics. 1975 Dec;81(4):683–704. doi: 10.1093/genetics/81.4.683. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Kirschner K., Bisswanger H. Multifunctional proteins. Annu Rev Biochem. 1976;45:143–166. doi: 10.1146/annurev.bi.45.070176.001043. [DOI] [PubMed] [Google Scholar]
- Mange A. P., Sandler L. A note on the maternal effect mutants daughterless and abnormal oocyte in Drosophila melanogaster. Genetics. 1973 Jan;73(1):73–86. doi: 10.1093/genetics/73.1.73. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Marshall T., Whittle J. R. Genetic analysis of the mutation female-lethal in Drosophila melanogaster. Genet Res. 1978 Oct;32(2):103–111. doi: 10.1017/s0016672300018590. [DOI] [PubMed] [Google Scholar]
- Norby S. A specific nutritional requirement for pyrimidines in rudimentary mutants of Drosophila melanogaster. Hereditas. 1970;66(2):205–214. doi: 10.1111/j.1601-5223.1970.tb02346.x. [DOI] [PubMed] [Google Scholar]
- Okada M., Kleinman I. A., Schneiderman H. A. Repair of a genetically-caused defect in oogenesis in Drosophila melanogaster by transplantation of cytoplasm from wild-type eggs and by injection of pyrimidine nucleosides. Dev Biol. 1974 Mar;37(1):55–62. doi: 10.1016/0012-1606(74)90169-9. [DOI] [PubMed] [Google Scholar]