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Citation
Cronmiller, C., Cline, T.W. (1986). The relationship of relative gene dose to the complex phenotype of the daughterless locus in Drosophila.  Dev. Genet. 7(): 205--221.
FlyBase ID
FBrf0044184
Publication Type
Research paper
Abstract

The daughterless (da) gene provides an essential maternally supplied component for Drosophila sex determination and dosage compensation. In this connection, it is required as a positive regulator of a female-specific master regulatory gene, Sex-lethal (Sxl). In addition, zygotic da gene function is required for male and female viability. Thus, the phenotype da is complex; it includes both maternal and zygotic aspects, as well as both sex-specific and nonsex-specific aspects. Assessment of wild-type da function has relied on the characterization of only a single leaky mutant da allele. In order to better understand the nature of this allele and the relationships between the various aspects of its complex phenotype, tandem duplications of both the mutant and wild-type da alleles were isolated and used in a dose study of this gene's function. Three conclusions were reached: 1) by the most stringent genetic criteria, the mutant da allele is a simple hypomorph, an allele with reduced but non-zero levels of wild-type functions; 2) since increased dose of da+ had no effect on viability or progeny sex ratio, this gene seems not to be a dose-sensitive element of the X/A ratio sex determination signal; and 3) expression of the maternal da+ allele does make a contribution to the nonsex-specific developmental processes that require zygotic da+ function; however, that contribution is clearly minor. In contrast, the zygotic genotype with respect to da appears to have no effect on the expression of Sxl+ in the zygote, the sex-specific process that requires maternal da+ function.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Dev. Genet.
    Title
    Developmental Genetics
    Publication Year
    1979-1999
    ISBN/ISSN
    0192-253X
    Data From Reference
    Aberrations (10)
    Alleles (1)
    Genes (2)