1. courtless, the Drosophila UBC7 Homolog, Is Involved in Male Courtship Behavior and Spermatogenesis
- Author
-
Daniel L. Segal, Ralph J. Greenspan, Galit Rosenfeld, and Sara Orgad
- Subjects
Male ,Molecular Sequence Data ,Mutant ,Gene Expression ,Biology ,Transfection ,medicine.disease_cause ,Animals, Genetically Modified ,Ligases ,P element ,Sexual Behavior, Animal ,Genetics ,Homologous chromosome ,medicine ,Animals ,Drosophila Proteins ,Cloning, Molecular ,Peptide Synthases ,Spermatogenesis ,Ubiquitins ,Gene ,Alleles ,Polytene chromosome band ,Mutation ,Base Sequence ,Sequence Homology, Amino Acid ,Gene map ,Homozygote ,Courtship ,Physical Chromosome Mapping ,Meiosis ,Ubiquitin-Conjugating Enzymes ,Insect Proteins ,Drosophila ,Female ,Drosophila Protein ,Research Article - Abstract
The courtless (col) mutation disrupts early steps of courtship behavior in Drosophila males, as well as the development of their sperm. Most of the homozygous col/col males (78%) do not court at all. Only 5% perform the entire ritual and copulate, yet these matings produce no progeny. The col gene maps to polytene chromosome band 47D. It encodes two proteins that differ in their carboxy termini and are the Drosophila homologs of the yeast ubiquitin-conjugating enzyme UBC7. The col mutation is caused by an insertion of a P element into the 3′ UTR of the gene, which probably disrupts translational regulatory elements. As a consequence, the homozygous mutants exhibit a six- to sevenfold increase in the level of the COL protein. The col product is essential, and deletions that remove the col gene are lethal. During embryonic development col is expressed primarily in the CNS. Our results implicate the ubiquitin-mediated system in the development and function of the nervous system and in meiosis during spermatogenesis.
- Published
- 2000
- Full Text
- View/download PDF