Courtship and copulation behaviors in Drosophila melanogaster males are regulated by sex-specific products from the gene fruitless (fru). Male-specific FRU proteins (FRU[superscript M]) are putative transcription factors of the BTB-ZnF family that likely act by controlling development and maintenance of the neural circuitry used during male sexual behavior. However, which neuronal characteristics are regulated by FRU[superscript M] is mostly unknown and how FRU[superscript M] neurons are grouped into circuits and the role that specific neuronal circuits play in sexual behavior has not been elucidated. I have identified a subset of FRU[superscript M] neurons that co-express the transcription factor, Engrailed (En). After fru[superscript M]-RNAi-induced targeted removal of FRU[superscript M] proteins from FRU[superscript M]/En neurons, males were impaired in their ability to initiate or maintain copulation. Further, I examined two characteristics, the initial projections and neurotransmitters used by FRU[superscript M]/En neurons. Males and females showed a difference in the neurochemistry of FRU[superscript M]/En neurons in the thoracic ganglia; this neurochemistry is disrupted in fru mutant males. For one cohort of serotonergic neurons in the abdominal ganglion that were previously shown to be dependent on FRU[superscript M] for expression of serotonin, I determined that FRU[superscript M] works in conjunction with other sex-specific genes, TAKEOUT (TO) and DOUBLESEX (DSX), to induce of serotonin expression in males; in females serotonin expression is repressed by DSX and TO. Finally, I performed a genetic screen for genes that interact with, or are downstream targets of, fru, dsx, or dissatisfaction (dsf). I assessed fertility, copulation success, and abdominal muscle development of EMS-mutagenized flies, resulting in one fly line in which homozygous mutant animals had a novel muscle phenotype. By genetic tests, the mutation was found to be allelic to string, which encodes a Cdc25- like phosphatase. Taken together, my research demonstrates that subsets of FRU[superscript M] neurons function in circumscribed circuits to regulate specific portions of sexual behavior, and that FRU[superscript M], along with other sex-specific genes, controls development of these neurons in part by determining neurochemistry. Further, FRU[superscript M] likely directs multiple downstream targets, in different subsets of neurons in which it is expressed, which collectively provide correct development of neural circuits underlying courtship and copulation behavior. / Graduation date: 2006

The fruitless (fru) gene in Drosophila melanogaster is a multifunctional gene having sex-specific functions in the regulation of male sexual behavior and sex-nonspecific functions affecting adult viability and external morphology. While much attention has focused on fru's sex-specific roles, little is known about its sex-nonspecific functions. The embryonic central nervous system (CNS) is a prime model system in which to study the genetic control of axonal outgrowth and proper CNS formation. I have examined fru's sex-nonspecific role in embryonic neural development. fru transcripts and FRU proteins from sex-nonspecific promoters are expressed beginning at the earliest stages of neurogenesis and subsequently in both neurons and glia. In embryos that lack most or all fru function, Fasciclin II- and BP102-positive axons appeared to defasciculate from their normal pathway and fasciculate along aberrant neuronal pathways, suggesting that one of fru's sex-nonspecific roles is to regulate axonal differentiation. I next examined whether the loss of fru function in FRU-expressing neuronal precursors causes neuronal fate change. Analysis of fru mutant embryos revealed a lack of Even-skipped (Eve) staining in Eve-expressing neurons, ectopic Eve staining in non-Eve-expressing neurons and mispositioned dorsal Eve-expressing neurons, which suggests that fru functions to maintain neuronal identity rather than to specify neuronal fate. In fru mutants these defects in axonal projections and in Eve staining were rescued by the expression of specific fru transgenes. To better understand fru's function in the formation of the embryonic CNS, I dissected out fru's function in neuron and glia through a genetic interaction study. fru genetically interacts in neurons with longitudinal lacking to make proper axonal projections. In addition, fru might be in the same genetic pathway as roundabout (robo), a repulsive guidance receptor, and commissureless, a downregulator of Robo, to ensure proper axonal pathfinding. Surprisingly, fru interacts with tramtrack and glial cells missing to repress neuronal differentiation in the lateral glia and with single-minded for the development of midline glia. Taken together, fru function is required for proper axonal pathfinding in neurons and for proper development of lateral and midline glia. / Graduation date: 2002

Thesis (Ph. D.)--University of Oregon, 2001. / Typescript. Includes vita and abstract. Includes bibliographical references (leaves 99-105). Also available for download via the World Wide Web; free to University of Oregon users.

Patterning of the body axes of the Drosophila embryo depends on maternally expressed genes, some of which function in the follicular epithelium of the developing egg chamber. Many such genes were identified in genetic screens for homozygous mutant females that produce abnormal embryos. However, mutations in zygotically required maternal effect genes are homozygous lethal, and therefore viable females cannot be recovered using this screening approach. This limitation can be overcome by generating homozygous mutant follicle cell clones in heterozygous females using a system that induces site-specific mitotic recombination events. However, to date, eggs produced from egg chambers with complete follicle cell clones cannot be directly identified. We have developed an eggshell marker for follicle cell clones using a dominant negative (DN) allele of the gene defective chorion (dec). Females with a single copy of this allele, decDN, lay collapsed eggs and are therefore sterile. Site-specific mitotic recombination events induced in females heterozygous for decDN and a mutation on the homologous chromosome arm result in homozygous mutant follicle cells that have lost decDN. Therefore, egg chambers with the entire follicular epithelium homozygous mutant generate intact eggs that can be unambiguously identified amongst otherwise collapsed eggs.

Thesis ( Ph.D.) -- McMaster University, 1998. / Includes bibliographical references (leaves 136-139). Also available via World Wide Web.

Thesis (Ph. D.)--University of Texas at Austin, 2008. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 121-139).

Undergraduate honors paper--Mount Holyoke College, 2008. Dept of Biological Sciences. / Non-Latin script record. Includes bibliographical references (leaves 85-92).

Thesis (Ph. D.)--University of Oregon, 2008. / Typescript. Includes vita and abstract. Includes bibliographical references (leaves 90-99). Also available online in Scholars' Bank; and in ProQuest, free to University of Oregon users.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 140-161).