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Genes and mechanisms underlying the development of dendrites in the central nervous system of the Drosophila embryoChwalla, Barbara January 2010 (has links)
No description available.
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Generating asymmetry in the developing Drosophila CNSKaltschmidt, Julia Anna January 2001 (has links)
No description available.
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The generation of cellular diversity in the Drosophila central nervous systemSchuldt, Alison Jean January 1999 (has links)
No description available.
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The molecular role of Bicaudal-C in Drosophila oogenesis /Chicoine, Jarred. January 2006 (has links)
Bicaudal-C (Bic-C) encodes a KH-type RNA binding protein required maternally for anterior patterning of the Drosophila oocyte and correct migration of the centripetal follicle cells. In Drosophila, premature translation of the germ-plasm determinant Oskar in Bic-C mutant oocytes suggests a function for Bic-C in post-transcriptional gene regulation. / Purification and microarray analysis of Bic-C containing ribonucleoprotein complexes revealed that Bic-C associates with multiple transcripts encoding functionally-related components of the Wnt/Frizzled/Dishevelled signaling pathway that regulate actin dynamics, in addition to its own mRNA. Using transgenic reporter constructs, Bic-C was demonstrated to destabilize its own mRNA via cis-acting 5' UTR elements. When auto-regulation was bypassed and Bic-C was over-expressed in the female germline, premature cytoplasmic streaming was induced, disrupting axial patterning through displacement of both Gurken (Grk) and oskar. These phenotypes can also be induced by disruption of the actin cytoskeleton with pharmacological agents and are similar to those described for hypomorphic mutant alleles of orb, which encodes a CPEB-like protein that promotes polyadenylation of target mRNAs. The Bic-C overexpression phenotypes require its RNA binding activity, are substantially enhanced by mutations affecting orb and poly(A) polymerase, and are suppressed by mutations affecting the deadenylase CCR4 and its accessory protein NOT3. Co-immunoprecipitation experiments demonstrate that Bic-C associates with components of the deadenylase complex and with components of an ER-associated RNP complex that includes Me31B, PABP and Trailer-hitch. The latter complex is involved in Grk exocytosis. Accordingly, Grk secretion is defective in Bic-C mutants. / Taken together, these results support a model whereby Bic-C antagonizes Orb function by negatively regulating the expression of Orb target mRNAs, through recruitment of the deadenylase machinery, that are involved in coordinating cytoplasmic movements. Furthermore, this work identifies a novel function of Bic-C in dorsal/ventral patterning by promoting Grk secretion.
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Initiation of developmental asymmetry by Drosophila Bic-D, DLis-1 and microtubulesSwan, Andrew. January 1999 (has links)
I have investigated the mechanisms by which developmental asymmetry arises, using oocyte determination in Drosophila melanogaster as a model system. The Bicaudal-D (Bic-D) gene is required early in oogenesis for the asymmetric localization of specific mRNAs and proteins and for the differentiation of an oocyte from one of a cluster of 16 interconnected germarial cells. To better understand how Bic-D functions in creating this asymmetry, I took two approaches. First, I examined the role of Bic-D in the asymmetric localization of mRNA and other cellular components during later oogenesis. Second, I molecularly and genetically characterized a gene that interacts with Bic-D in oocyte determination. To determine the role of Bic-D in later oogenesis, I used an inducible source of Bic-D activity to selectively rescue the block at oocyte determination in Bic-D null mutants. Using this system, I find that Bic-D is indeed required in the later stages of oogenesis for the localization of specific mRNAs at both the anterior and posterior of the oocyte. Bic-D is also required for oocyte growth and nuclear positioning, processes which also depend on microtubules. / In the second part of this thesis, I describe the characterization of a Bic-D interacting gene which I have identified as the Drosophila homologue of the human Lissencephaly-1 (Lis-1) gene, DLis-1. Human Lis-1 is the causative gene for Miller-Dieker Syndrome and is required for neuronal migration in the developing brain, while fungal homologues have been implicated in dynein dependent nuclear migration. Like Bic-D , DLis-1 is essential for oocyte determination and for intracellular localization throughout oogenesis. DLis-1 is required for correct positioning of the oocyte nucleus, and appears to function upstream of dynein in this process. Immunolocalization studies suggest that DLis-1 functions as part of a cortical anchor that links microtubules and the oocyte nucleus, via dynein and microtubules, to the cell cortex. DLis-1 and Bic-D are also required for nuclear positioning during neural development in Drosophila, supporting a model in which the neuronal migration defects in Miller-Dieker Syndrome are due to a disruption of dynein/Lis-1 dependent nuclear migration.
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Developing an eggshell marker based on a dominant female sterile mutation for the identification of complete follicle cell clones in Drosophila melanogasterEleiche, Aliaa Abdel-Salam. January 2006 (has links)
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.
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The evolution of sex-related traits and speciation in Drosophila /Civetta, Alberto. January 1998 (has links)
Thesis ( Ph.D.) -- McMaster University, 1998. / Includes bibliographical references (leaves 136-139). Also available via World Wide Web.
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Determining roles of the SUN domain proteins klaroid and Dspag4 in Drosophila developmentKracklauer, Martin Paul, January 1900 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 2008. / Vita. Includes bibliographical references.
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Steroid hormone receptor regulation of neuronal pruning and outgrowth in the Drosophila central nervous system /Brown, Heather L. D. January 2007 (has links)
Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 121-139).
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<>.Rahman, Ishita. January 2008 (has links) (PDF)
Undergraduate honors paper--Mount Holyoke College, 2008. Dept of Biological Sciences. / Non-Latin script record. Includes bibliographical references (leaves 85-92).
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