Browsing by Subject "Drosophila--Genetics"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
Item Comparative genomics and molecular population genetics of Drosophila male reproductive genes(2004) Wagstaff, Bradley Jon; Mueller, Ulrich G.; Begun, David J.DNA sequence data from male reproductive genes in numerous taxa have shown that these genes typically evolve more rapidly than other genes, often as a result of directional selection. In the genus Drosophila, the rapidly evolving male accessory gland protein genes (Acps) of melanogaster subgroup flies have contributed to this observation. Acps are small proteins that are transferred to females during mating as a major component of the seminal fluid and are considered agents of chemical communication between the sexes. Acps are known to contribute to normal ovulation and sperm storage, as well as increase oviposition rates and reduce female receptivity. Thus, Acps are considered likely targets of directional selection because of their potential roles in postcopulatory sexual selection and antagonistic coevolution between the sexes. Outside of melanogaster subgroup Acps, little is known about the evolutionary biology of male reproductive genes in Drosophila. For example, the male testis contains a richly diverse transcriptome but no studies have explored the evolutionary dynamics of a large set of testis-expressed genes. If clear differences in the evolutionary dynamics of different classes of male reproductive genes exist, empirical documentation of these differences will help identify the specific evolutionary forces at work. Additionally, mating systems differ between Drosophila species, potentially affecting the evolutionary dynamics of Acps across lineages. Comparative analyses of Acps from species with different mating systems are needed to address this issue. Finally, if Acps are generally rapidly evolving in Drosophila species, comparative analyses of orthology and Acp gene loss/gain are needed to determine how Acps respond to persistent directional selection across lineages. The data presented here aim to address these questions. Included are polymorphism and divergence data from 56 genes of Drosophila arizonae and D. mojavensis, repleta group species with mating systems that differ dramatically from melanogaster subgroup flies. The sample includes 19 Acps, 31 testis-expressed genes, and six more evenly expressed genes. Comparative genomics analyses of D. melanogaster-D. mojavensis male reproductive genes and D. melanogaster-D. pseudoobscura Acps are also presented to address questions of functional conservation across lineages.Item Establishing a Drosophila model for Angelman syndrome(2007) Wu, Yaning, 1974-; Fischer, Janice AnnDrosophila models for human diseases have helped in advancing our knowledge on human diseases and the discovery of potential treatments. Angelman syndrome is a rare neurological disorder that results in severe mental retardation and loss of motor coordination. The disease is caused by loss-of-function mutations in the UBE3A gene encoding a HECT domain ubiquitin protein ligase. Drosophila dube3a is the fly homolog of human UBE3A and their protein products share ~55% similarity in amino acid sequence along the entire length of the proteins. My goal was to develop a Drosophila AS model that will allow us to identify the AS-associated substrate(s) of the Drosophila UBE3A homolog and ultimately, to determine why the lack of UBE3A protein causes Angelman syndrome in humans. Dube3a is present in the embryonic, larval and adult central nervous system, including the adult mushroom bodies, which is the center for learning and memory. I have generated dube3a knock-out flies and they appear normal externally, but display abnormal locomotor behaviors. Flies that overexpress wild-type dube3a in the nervous system also display locomotion defects, and these overexpression phenotypes are dependent on the presence of a conserved cysteine residue essential for HECT domain E3 enzymatic activity. Targeted overexpression of dube3a in the eye, the wing, or ubiquitously causes rough eyes, curly wings and lethality, respectively. These morphological abnormalities in the eye or wing depend on the critical catalytic cysteine of Dube3a. Overexpression of mutant dube3a carrying AS-associated point mutations does not elicit such defects, suggesting they act as loss-of-function mutants. Taken together, dube3a mutants are a candidate fly model for Angelman syndrome, and the flies that overexpress dube3a in the eye or wing are useful for genetic screens to identify the elusive UBE3A substrates relevant to Angelman syndrome.