Errata is pasted onto back end paper. / Includes bibliographical references (26 leaves). / 115, [68] leaves, [8] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This study entailed work towards the isolation of the pbl gene and preliminary characterisation of a candidate pbl transcript. Plasmid rescue of the genomic DNA flanking the inserted P element led to the isolation of a third candidate p61 cDNA, the 1A cDNA. This data suggests that the IA cDNA is encoded by the p61 gene. / Thesis (Ph.D.)--University of Adelaide, Dept. of Genetics, 1998

No description available.

The polyhomeotic (ph) locus of Drosophila melanogaster has been characterized genetically. Early studies showed that ph is a member of the Polycomb (Pc) group. These genes have similar phenotypes and are required for normal segment determination. Recent analyses of amorphic ph mutations show that the ph locus is complex, has a strong maternal effect and plays a role in cuticular development. To test the function of ph at the molecular level, the cloning of the ph locus was undertaken. One strain had been shown to contain a P element insertion near ph. A genomic library was prepared from this strain and a recombinant phage containing this P element insertion was isolated by transposon tagging. The DNA flanking the insertion was used as a starting point for a chromosomal walk. A series of overlapping phage spanning 170 kilobases was isolated. Southern blot analysis was used to determine the locations of important deficiency breakpoints within the region covered by the walk. A distance of approximately 35 kb was shown to separate the two deficiency breakpoints which include ph. This interval was found to contain rearrangements in four of the seven ph alleles which were examined by Southern blot analysis. The interval also contains a repeated sequence. The relationship between the genetic and molecular structure of ph is discussed. / Science, Faculty of / Zoology, Department of / Graduate

Mutagen-sensitive (mus) mutations in Drosophila melanogaster render developing flies hypersensitive to the lethal effects of DNA-damaging agents. In general, mus mutations identify DNA repair-related genes. In this study, 5 new second chromosome mus mutations (mus205B¹, mus208B¹, mus209B¹, mus210B¹ and mus211B¹), selected on the basis of sensitivity to methyl methanesulfonate (MMS), were characterized using a variety of genetic tests. One test measured the MMS-sensitivity of double mutant mus strains compared to their component single mutants. Mutant interactions were examined in 8 double mus and in 2 triple mus strains containing combinations of mus201D¹, mus205B¹, mus208B¹, mus210B¹ and mus211B¹ (or mus211B²). These analyses have revealed predominantly synergistic and epistatic responses to MMS. Taken together with the findings of previous genetic and biochemical studies of Drosophila mus strains, these results suggest that 3 major repair pathways may operate in flies to correct damage caused by MMS. Mutagen cross-sensitivity data and the results of the interaction studies suggest that mus mutations might serve as rapid and sensitive bioassays of somatic genotoxicity caused by mutagens and carcinogens. To explore this possibility, a simple mutagen test system was devised employing triple mutant mus strains. One strain (mus208B¹ mus210B¹ mus211B²) was tested for sensitivity to 14 mutagens/carcinogens and 2 non-carcinogens. Eleven of the mutagens/carcinogens were readily detected as genotoxic. Both non-carcinogens were non-genotoxic. These preliminary results demonstrate the feasibility (and some limitations) of the proposed somatic genotoxicity assay and emphasize the need for further test validation using a larger chemical data base. The temperature-sensitive lethal mutation mus209B¹ was subjected to extensive genetic analyses and to temperature shift experiments during development. This locus was found to encode a product(s) that (1) is essential for viability at virtually all pre-imaginal developmental stages (the latter half of pupation appears to be an exception), (2) is necessary for wildtype levels of resistance to the genotoxic effects of MMS and ionizing radiation, and (3) is required for female fertility. Confirmation of the pleiotropic nature of this mutation was obtained by meiotic and cytogenetic mapping studies and by complementation tests with a series of allelic mutations. The mus209B¹ phenotypes are similar to ones conferred by mutations in Drosophila and yeast that disrupt various aspects of chromosome metabolism. In this context, some possible roles for mus209B¹ are discussed. / Science, Faculty of / Zoology, Department of / Graduate

Damage to DNA from a variety of sources can lead to damaged proteins, genomic instability, aneuploidy, and cancer. It is therefore essential to repair DNA damage, and to do so a variety of DNA repair mechanisms have evolved. One of the repair mechanisms, known as homologous recombination (HR) repair, uses an undamaged sister chromatid as a template to make error free repairs to double-strand (ds) DNA breaks. While many proteins are involved in HR, this work focuses on testing the interactions of a subset of these proteins known as the Rad51 paralogs. The goal of this study is to determine if the putative Rad51 paralogs in Drosophila melanogaster are sufficiently conserved as to function in the same manner as their human counterparts. This research is part of a larger project to determine if Drosophila melanogaster is a good model organism for studying HR in humans (Hs). The D. melanogaster Rad51 gene, and its four paralogs Spn D, Spn B, Rad51D, XRCC2 (the last 2 identified by sequence homology), and human hsRad51D and hsXRCC2, were cloned into Invitrogen's TOPO protein expression vector. When induced with IPTG, the resulting fusion proteins contains either aN-terminal Xpress TM epitope or a C-terminal V5 epitope. The fusion proteins were used in immunoprecipitation assays with antibodies against the epitope tags to test for proteinprotein interactions. While many of the assays were inconclusive and are still being optimized, the interaction of the C-terminally tagged dmXRCC2 with theN-terminally tagged hsRad51D gave a positive result. This single interspecies result suggests that homologous recombination is highly conserved between D. melanogaster and humans.

Understanding the biological basis of behavior is crucial for gaining insights into human nature, treating behavioral disorders and improving overall well-being. Efforts to understand the biological basis of behavior have largely emphasized the role of neurons. However, examples across life show that behavior can occur in lieu of or in cell types outside of neurons. This thesis presents work exploring the mechanisms underlying multiple behaviors using the model system Drosophila melanogaster. Chapter 2 provides evidence for the influence of glia on courtship, aggression, and sleep. Chapter 3 characterizes a Drosophila model of autism spectrum disorder, finding that genetic neuronal manipulation of a single gene can cause pathologies beyond the nervous system. Chapter 4 investigates the connection between sleep behavior and oxidative stress response, demonstrating metabolism as a probable mediator of this relationship. Altogether, this work supports a wider definition for the biological basis of behavior.

No description available.

For animals to walk properly, motor neurons (MNs) need to reach their target muscles in the leg and they need to arborize properly. Cell adhesion molecules (CAMs) have pivotal roles in a variety of neural development processes including arborization. Two Immunoglobulin Super Family (IgSF) CAMs, DIP-α and its interacting partner Dpr10, have been shown to play key roles in leg MN arborization in flies. DIP-α is expressed by three leg MNs and dpr10 is expressed by leg muscles. When either DIP-α or dpr10 are removed in flies MNs reach their target but fail to arborize their branches. Interestingly, DIP-α and Dpr10 have some of the highest binding affinities relative to other DIPs and Dpr interacting pairs. Therefore, in this thesis I ask how important are these relatively high affinities and do the MNs have different affinity requirements? I show that decreasing and increasing the affinity between these two proteins in vivo has adverse effects on MN arborization and that different MNs rely on different thresholds of DIP-α::dpr10 binding affinities to arborize properly. Based on these experiments, I then ask how DIPs and Dprs interact when they are co-expressed by the same neuron. Here I provide evidence that altering the ratio of DIP-a::dpr10::dpr6 can inhibit DIP-α’s ability to bind in trans with Dpr10. Furthermore, together with Dr. Nick Morano in the Shapiro lab, we show that DIP-α has a longer linker domain compared to DIPs that are not able to bind in cis and that removing this linker domain in vivo phenocopies some of the effects seen by removing co-expressed dpr6 or dpr10 in DIP-α MNs. Therefore, although DIP-α and its partners Dpr6 and Dpr10 are expressed in MNs, relative concentrations and cis interactions in MNs dictate how DIP-α interacts in trans with Dpr10. Together, this thesis provides a better understanding as to how interactions between CAMs can be modified via affinities, concentration, and co-expression in vivo to ultimately shape axon morphology of Drosophila leg MNs.

A thesis submitted to the Faculty of Science, University of the Witwatersrand, Johannesburg for the Degree of Doctor of Philosophy. / This thesis reports on the investigation of two genetic aspects of Southern African populations of Drosophila Melanogaster: the " family of transposable elements and the allelic variation present in several enzyme systems. (Abbreviation abstract) / Andrew Chakane 2018

Aging is a biological process that has many detrimental effects due to the accumulation of oxidative damage to key biomolecules due to the action of free radicals. Methionine sulfoxide reductase (Msr) functions to repair oxidative damage to methionine residues. Msr comes in two forms, MsrA and MsrB, each form has been shown to reduce a specific enantiomer of bound and free oxidized methionine. Effects of Msr have yet to be studied in the major developmental stages of Drosophila melanogaster despite the enzymes elevated expression during these stages. A developmental timeline was determined for MsrA mutant, MsrB mutant, and double null mutants against a wild type control. Results show that the Msr double mutant is delayed approximately 20 hours in the early/mid third instar stage while each of the single mutants showed no significant difference to the wild type. Data suggests that the reasoning of this phenomenon is due to an issue gaining mass. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2013. / FAU Electronic Theses and Dissertations Collection