Skip to main content
Genetics logoLink to Genetics
. 1986 Jul;113(3):641–663. doi: 10.1093/genetics/113.3.641

A Female-Specific Lethal Lesion in an X-Linked Positive Regulator of the Drosophila Sex Determination Gene, SEX-LETHAL

Thomas W Cline 1
PMCID: PMC1202860  PMID: 3089868

Abstract

Characterization of a partial-loss-of-function, female-specific lethal mutation has identified an X-linked genetic element ( 1-34.3; 10B4) that functions as a positive regulator of Sxl, a central gene controlling sex determination in Drosophila melanogaster . The name, sisterless-a, was chosen both to suggest functional similarities that exist between this gene and another positive regulator of Sxl, the maternally acting gene daughterless (da), and also to highlight an important difference; namely, that in contrast to da, it is the zygotic rather than maternal functioning of sis-a that is involved in its interaction with Sxl. As with da, the female-specific lethal phenotype of sis-a is suppressed both by SxlM#1, a gain-of-function mutant allele of the target gene, and, to a lesser extent, by a duplication of Sxl+. Mutations at sis-a, da and Sxl display female-specific dominant synergism, each enhancing the others' lethal effects. The allele specificity with respect to Sxl of these dominant interactions indicates that sis-a and da affect the same aspect of Sxl regulation. As with previous studies of da and Sxl, the masculinizing effects of loss of sis-a function are generally obscured by lethal effects, presumably related to upsets in dosage compensation. The masculinizing effects can be dissociated from lethal effects by analysis of triploid intersexes (XX AAA) or by analysis of diploid females who are also mutant for autosomal genes known to be required for the transcriptional hyperactivation associated with dosage compensation in males. Analysis of foreleg development shows that intersexuality generated by sis-a is of the mosaic type: At the level of individual cells, only male or female development is observed, never an intermediate sexual phenotype characteristic of true intersexes. Sexual development of diplo-X germline and somatic clones of sis-a tissue generated by mitotic recombination during larval stages is normal, as is the sexual phenotype of homozygous sis-a escapers. Considered in their totality, these results indicate that sis-a functions early in development to help establish the activity state of Sxl and thereby initiate the sexual pathway commitment, rather than functioning later in the processes by which Sxl maintains and expresses the sex determination decision.

Full Text

The Full Text of this article is available as a PDF (1.5 MB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Baker B. S., Belote J. M. Sex determination and dosage compensation in Drosophila melanogaster. Annu Rev Genet. 1983;17:345–393. doi: 10.1146/annurev.ge.17.120183.002021. [DOI] [PubMed] [Google Scholar]
  2. Cline T. W. A sex-specific, temperature-sensitive maternal effect of the daughterless mutation of Drosophila melanogaster. Genetics. 1976 Dec;84(4):723–742. doi: 10.1093/genetics/84.4.723. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Cline T. W. The interaction between daughterless and sex-lethal in triploids: a lethal sex-transforming maternal effect linking sex determination and dosage compensation in Drosophila melanogaster. Dev Biol. 1983 Feb;95(2):260–274. doi: 10.1016/0012-1606(83)90027-1. [DOI] [PubMed] [Google Scholar]
  4. Cline T. W. Two closely linked mutations in Drosophila melanogaster that are lethal to opposite sexes and interact with daughterless. Genetics. 1978 Dec;90(4):683–698. doi: 10.1093/genetics/90.4.683. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Morata G., Ripoll P. Minutes: mutants of drosophila autonomously affecting cell division rate. Dev Biol. 1975 Feb;42(2):211–221. doi: 10.1016/0012-1606(75)90330-9. [DOI] [PubMed] [Google Scholar]

Articles from Genetics are provided here courtesy of Oxford University Press

RESOURCES