@article{87661,
  keywords = {Animals, Base Sequence, Drosophila, signal transduction, Mutation, Molecular Sequence Data, Promoter Regions, Genetic, Sequence Homology, Nucleic Acid, Binding Sites, Genes, Reporter, Conserved Sequence, Female, Male, Gene Expression Regulation, Developmental, Embryo, Nonmammalian, Animals, Genetically Modified, Drosophila melanogaster, Drosophila Proteins, RNA-Binding Proteins, Sex Determination Processes, 5{\textquoteright} Untranslated Regions},
  author = {Timothy Morgan Jinks and Gretchen Calhoun and Paul Schedl},
  title = {Functional conservation of the sex-lethal sex determining promoter, Sxl-Pe, in Drosophila virilis.},
  abstract = { The primary sex determination signal in Drosophila melanogaster, the ratio of X chromosomes to autosomes, sets the activity state of the switch gene, Sex-lethal ( Sxl), by regulating the establishment promoter, m-Sxl-Pe. We have identified and characterized the establishment promoter, v-Sxl-Pe, of the distantly related species Drosophila virilis. Like melanogaster, the virilis Sxl-Pe is organized into four sub-domains: the Sxl-Pe mRNA leader and exon E1 of Sxl protein, the core promoter, the sex-specific element and the augmentation element. The core promoter and sex-specific element of v-Sxl-Pe show considerable sequence similarity to m-Sxl-Pe and contain target sites for components of the X/A signaling system. While the augmentation element of v-Sxl-Pe also has sequence motifs that could function as target sites for the X/A signaling system, it shows little similarity to the melanogaster augmentation element. Functional studies reveal that v-Sxl-Pe drives sex-specific expression in D. melanogaster embryos and that the activity of the virilis promoter is controlled by known components of the melanogaster X/A counting system. Although v-Sxl-Pe responds appropriately to the melanogaster sex determination signal, it is less active than Sxl-Pe from melanogaster. Unexpectedly, the reduced activity is due to differences in the activity of the conserved core promoter, while the non-conserved augmentation element functions effectively. These findings suggest that low-affinity target sites for the X/A counting system are critical for the functioning of Sxl-Pe. },
  year = {2003},
  journal = {Dev Genes Evol},
  volume = {213},
  pages = {155-65},
  month = {05/2003},
  issn = {0949-944X},
  doi = {10.1007/s00427-003-0304-1},
  language = {eng},
}