The genetic factors controlling Mixed Function Oxidase (MFO) Activity and malathion resistance was studied in the larva and the adult of a malathion resistant strain of Drosophila melanogaster. In addition, the developmental expression and tissue localization of high MFO activity was characterized in the larva and the adult. Microsomal extracts from a strain with a resistant second chromosome were found to have increased amounts of protein with a relative molecular mass of 52 kD, while a strain with a resistant third chromosome was found to have increased amounts of proteins with relative molecular masses of 51 and 55 kD in the microsomal extract. MFO activity associated with a strain with a resistant second chromosome was found to be most concentrated in the intestine and abdominal wall of the imago, while found primarily in the malpigian tubules and the fat body of the larva. The mapping of genes on the second chromosome associated with larval resistance to malathion suggested two loci, a major resistance gene at 2-64 cM and a second minor resistance gene. The mapping of genes on the second chromosome associated with adult resistance again suggested two loci, one at 2-64 cM and a second just to the left of the marker black (48.5 cM). The mapping of genes on the second chromosome associated with high PNA demethylase activity (an MFO activity) in the adult suggested a locus at 2-64 cM and a second between 54.5 and 60.0 cM. The locus at 2-64 cM and a third locus between 48.5 and 51 cM was found to be associated with high 7-EC hydroxylase activity ( a second MFO activity) in the adult. / Thesis / Master of Science (MS)

Cheng, Tat Cheung. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 181-188). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 132-151).

Thesis (Ph. D.)--University of Washington, 2000. / Vita. Includes bibliographical references (leaves 157-170).

A dissertation submitted to the Faculty of Science, University of the Witwatersrand, in fulfillment of the requirements for the degree Master of Science. July, 2014 / Drosophila melanogaster, a key model organism, has cognates of over 70% of human disease genes. This has created opportunities in the development of treatments for life threatening illnesses like cancer. Mutations on the p53 tumour suppressor protein, which is an activator of apoptosis, are common in many cancers. In mammals, p53 interacts with the Retinoblastoma Binding Protein 6 (RBBP6) which enhances the activity of MDM2, the prototypical negative regulator of p53, that is absent in invertebrates. In the absence of MDM2 the Drosophila RBBP6 homolog, SNAMA, through its DWNN Catalytic Module (DCM), is suspected to play an important role in the regulation of p53, probably via the ubiquitin proteasome pathway. Through bioinformatics analyses, and experimental analysis of transcripts, this study has shown the existence of two isoforms of SNAMA named here SNAMA A and SNAMA B for the long and short isoforms, respectively. SNAMA B appears to be expressed after genotoxic stress (DNA damage) in adults as well as during embryonic development. Recombinant protein expression in bacterial and yeast systems as well as HIS-tag chromatography and Western blot analyses were used to investigate interactions with Dmp53. Due to poor expression of recombinant Dmp53 protein in both prokaryotic and eukaryotic systems and unreliable commercial antibodies, it was impossible to complete interaction studies. Overall, these studies show that the SNAMA isoforms may play important roles during development and in response to DNA damage.

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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.

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