+publisher:"University of Kansas" +contributor:("Lundquist, Erik A.")

University of Kansas

1. Blankenfeld, Bryce R. Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites.

Degree: MS, Neurosciences, 2017, University of Kansas

URL: http://hdl.handle.net/1808/26897

► Alzheimer’s disease is the 6th leading cause of death in the U.S. and the cost of care is billions of dollars per year. Tau aggregation… (more)

Subjects/Keywords: Neurosciences; Alzheimer's disease; Aspergillus nidulans; Secondary Metabolites; Tau Aggregation inhibitors

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APA (6^th Edition):

Blankenfeld, B. R. (2017). Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites. (Masters Thesis). University of Kansas. Retrieved from http://hdl.handle.net/1808/26897

Chicago Manual of Style (16^th Edition):

Blankenfeld, Bryce R. “Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites.” 2017. Masters Thesis, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/26897.

MLA Handbook (7^th Edition):

Blankenfeld, Bryce R. “Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites.” 2017. Web. 28 Jan 2021.

Vancouver:

Blankenfeld BR. Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites. [Internet] [Masters thesis]. University of Kansas; 2017. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/26897.

Council of Science Editors:

Blankenfeld BR. Characterization of a Novel Tau Aggregation Inhibitor Isolated from Fungal Secondary Metabolites. [Masters Thesis]. University of Kansas; 2017. Available from: http://hdl.handle.net/1808/26897

University of Kansas

2. Andres, Erin M. Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach.

Degree: MA, Child Language, 2018, University of Kansas

URL: http://hdl.handle.net/1808/27806

► Specific language impairment (SLI) is characterized by a delay in the mastery of language despite average or above average nonverbal intelligence (IQ). There are multiple… (more)

Subjects/Keywords: Genetics; Language; genetic linkage; language phenotypes; linkage analysis; pedigree; reading phenotypes; specific language impairment

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APA (6^th Edition):

Andres, E. M. (2018). Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach. (Masters Thesis). University of Kansas. Retrieved from http://hdl.handle.net/1808/27806

Chicago Manual of Style (16^th Edition):

Andres, Erin M. “Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach.” 2018. Masters Thesis, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/27806.

MLA Handbook (7^th Edition):

Andres, Erin M. “Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach.” 2018. Web. 28 Jan 2021.

Vancouver:

Andres EM. Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach. [Internet] [Masters thesis]. University of Kansas; 2018. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/27806.

Council of Science Editors:

Andres EM. Mapping Chromosomal Loci in Specific Language Impairment: A Pedigree-Focused Approach. [Masters Thesis]. University of Kansas; 2018. Available from: http://hdl.handle.net/1808/27806

University of Kansas

3. Voss, Kellen R. Modulation of Tau Dysfunction In Vitro.

Degree: PhD, Molecular Biosciences, 2011, University of Kansas

URL: http://hdl.handle.net/1808/8397

► The microtubule associated protein tau is a causative factor in a class of neurodegenerative diseases termed tauopathies. Alzheimer's disease (AD) is the most prevalent tauopathy.… (more)

▼ The microtubule associated protein tau is a causative factor in a class of neurodegenerative diseases termed tauopathies. Alzheimer's disease (AD) is the most prevalent tauopathy. In AD, natively unfolded, tau becomes hyperphosphorylated, and undergoes a conformational change allowing hexapeptide regions near microtubule binding repeat region 2 to aggregate into fibers. Tau exists in neurons as six alternatively spliced isoforms. The expression levels of tau are not changed in many tauopathies; however, various levels of each isoform can be included in aggregation depending on the disease. This indicates post-translational modifications or interactions with other proteins causes certain tau isoforms to be included in or excluded from these insoluble inclusions. Tau functions by assembling and stabilizing microtubules and is regulated by phosphorylation. In AD, the phosphorylation state of tau is altered so the affinity for microtubules is reduced; however, how changes in tau phosphorylation affect polymerization of tau isoforms is not fully understood. Abnormal aggregation of protein in a cell is mediated by molecular chaperones. A class of molecular chaperones, heat shock proteins, is upregulated in response to cellular stress. The most widely involved is heat shock protein 70 (Hsp70), which has upregulated and inversely proportional protein levels to tau aggregation in hippocampal neurons. Hsp70 can increase tau solubility in cells; however, it is unknown if Hsp70 can act directly on tau to prevent its dysfunction. This dissertation explores how phosphorylation with GSK-3β, the major kinase believed to be involved in tau hyperphosphorylation, and interactions with Hsp70, affect tau dysfunction (polymerization) and function (microtubule binding and assembly). Tau isoforms were found to be differentially affected by phosphorylation, as indicated by differences in their overall polymerization and various morphologies. Likewise, tau phosphorylation differentially affected their affinity for stabilized microtubules. Tau isoform polymerization was inhibited by Hsp70, with various concentrations of Hsp70 needed for complete inhibition. Finally, while Hsp70 altered the microtubule assembly properties of tau isoforms, each individual isoform was able to assemble microtubules robustly. Taken together, this dissertation shows tau isoforms respond differently to modifications and interaction with Hsp70, indicating each isoform could play a specific role in the progression of tauopathies. Advisors/Committee Members: Gamblin, Truman C. (advisor), Kelly, Paul T (advisor), Lundquist, Erik A. (cmtemember), Azuma, Yoshiaki (cmtemember), Davido, David O. (cmtemember), Kelly, John (cmtemember).

Subjects/Keywords: Molecular biology; Alzheimer's disease; Gsk-3β; Hsp70; Phosphorylation; Tau; Tauopathies

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Voss, K. R. (2011). Modulation of Tau Dysfunction In Vitro. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/8397

Chicago Manual of Style (16^th Edition):

Voss, Kellen R. “Modulation of Tau Dysfunction In Vitro.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/8397.

MLA Handbook (7^th Edition):

Voss, Kellen R. “Modulation of Tau Dysfunction In Vitro.” 2011. Web. 28 Jan 2021.

Vancouver:

Voss KR. Modulation of Tau Dysfunction In Vitro. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/8397.

Council of Science Editors:

Voss KR. Modulation of Tau Dysfunction In Vitro. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/8397

University of Kansas

4. Norris, Adam D. WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS.

Degree: PhD, Molecular Biosciences, 2011, University of Kansas

URL: http://hdl.handle.net/1808/7692

► The growth cone of a developing axon senses and responds to extracellular cues resulting in the migration of the growth cone and thus the axon… (more)

Subjects/Keywords: Neurosciences

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APA (6^th Edition):

Norris, A. D. (2011). WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7692

Chicago Manual of Style (16^th Edition):

Norris, Adam D. “WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/7692.

MLA Handbook (7^th Edition):

Norris, Adam D. “WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS.” 2011. Web. 28 Jan 2021.

Vancouver:

Norris AD. WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/7692.

Council of Science Editors:

Norris AD. WATCHING NEURONS GROW: GUIDANCE RECEPTORS, SIGNAL TRANSDUCTION MACHINERY AND CYTOSKELETAL REGULATORS AFFECT GROWTH CONE MORPHOLOGY AND DYNAMICS IN C. ELEGANS. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/7692

University of Kansas

5. Xu, Jiang. Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber.

Degree: PhD, Molecular Biosciences, 2011, University of Kansas

URL: http://hdl.handle.net/1808/8404

► The Drosophila egg chamber provides an excellent system in which to study the specification and differentiation of epithelial cell fates because all of the steps,… (more)

▼ The Drosophila egg chamber provides an excellent system in which to study the specification and differentiation of epithelial cell fates because all of the steps, starting with the division of the corresponding stem cells (called follicle stem cells or FSCs), have been well described and occur many times over in a single ovary. Here I investigate the role of the small Rab11 GTPase in follicle stem cells (FSCs) and in their differentiating daughters, which include main body epithelial cells, stalk cells and polar cells. I show that rab11-null FSCs maintain their ability to self renew, even though previous studies have shown that FSC self renewal is dependent on maintenance of E-cadherin-based intercellular junctions, which in many cell types, including Drosophila germline stem cells, requires Rab11. I also show that rab11-null FSCs give rise to cells that enter polar, stalk, and epithelial cell differentiation pathways, but that none of the cells are able to complete their differentiation programs and that the epithelial cells undergo premature programmed cell death. Finally I show, through the induction of rab11-null clones at later points in the differentiation program, that Rab11 suppresses tumor-like epithelial cell growth. Thus, rab11-null epithelial cells arrest differentiation early, assume an aberrant cell morphology, delaminate from the epithelium, and invade the neighboring germline cyst. These phenotypes are associated with defects in E-cadherin localization and a general loss of cell polarity. While previous studies have revealed tumor suppressor or tumor suppressor-like activity for regulators of endocytosis, this study is the first to identify such activity for regulators of endocytic recycling. This study also supports the recently emerging view that distinct mechanisms regulate junctional stability and plasticity in different tissues. Advisors/Committee Members: Cohen, Robert S. (advisor), Corbin, Victoria L. (cmtemember), Ward, Robert E. (cmtemember), Lundquist, Erik A. (cmtemember), Gleason, Jennifer M. (cmtemember).

Subjects/Keywords: Developmental biology; Molecular biology; Cellular biology; Cell differentiation; Cell polarity; Drosophila oogenesis; Rab11; Stem cells; Tumor supressor gene

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Xu, J. (2011). Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/8404

Chicago Manual of Style (16^th Edition):

Xu, Jiang. “Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/8404.

MLA Handbook (7^th Edition):

Xu, Jiang. “Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber.” 2011. Web. 28 Jan 2021.

Vancouver:

Xu J. Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/8404.

Council of Science Editors:

Xu J. Multiple Distinct Roles for the Rab11 GTPase in the Somatic Cells of the Drosophila Egg Chamber. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/8404

University of Kansas

6. Mattingly, Brendan Christopher. EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal.

Degree: PhD, Molecular Biosciences, 2011, University of Kansas

URL: http://hdl.handle.net/1808/7832

► The goal of this work is to understand how cells form and maintain tubular shapes. The protein EXC-5 is necessary for a small tubular structure… (more)

▼ The goal of this work is to understand how cells form and maintain tubular shapes. The protein EXC-5 is necessary for a small tubular structure in Caenorhabditis elegans to maintain its shape. C. elegans is a small, easily manipulable, genetically tractable, and transparent nematode with a unicellular excretory canal system. The C. elegans excretory canal cell is a long "H"-shaped tubular structure that serves as the osmoregulatory organ for the animal. EXC-5 is a guanine nucleotide exchange factor (GEF). GEF proteins work by binding to GDP-bound small GTPases and facilitating the exchange of GDP with GTP, thus activating the GTPase. The activated GTPases are effectors themselves and interact with numerous other proteins to direct various cellular processes. In this dissertation I discuss the various methods by which I examined how EXC-5 functions in order to maintain the tubular structure of the excretory canal. I describe an EMS non-complementation screen to identify new alleles of EXC-5, an EMS screen to identify genetic enhancers of EXC-5, methods to create an excretory canal-specific RNAi strain of C. elegans, the genetic interactions between exc-5, cdc-42, mig-2, ced-10 and other genes, the organization of subcellular organelles within the canal cell and in exc-5 mutants, the generation of intein containing proteins to create conditional alleles, and the generation of antibodies that bind to EXC-5. The data from these studies lead to a model of tubular maintenance where the sorting of material to the apical surface is only required at certain points along the canal where it is undergoing significant restructuring because of growth or physical damage. When exc-5 is mutant, materials are not efficiently sorted to the apical surface where they are needed to maintain the apical surface. Failure of the actin network under osmotic pressure from fluid within the lumen causes cysts to form in the canal cell. When EXC-5 is overexpressed, sorting to the apical surface is enhanced at the expense of sorting to the basal surface. This leads to an inability of the basal surface to adhere to the basement membrane and grow out, causing a convoluted tubule phenotype. Advisors/Committee Members: Buechner, Matthew J. (advisor), Cohen, Robert (cmtemember), Lundquist, Erik A. (cmtemember), Neufeld, Kristi L. (cmtemember), Suprenant, Kathy (cmtemember), Martin, Craig (cmtemember).

Subjects/Keywords: Cellular biology; Genetics; Developmental biology; Elegans; Endosome; Fgd; Morphogenesis; Trafficking; Tubulogenesis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mattingly, B. C. (2011). EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7832

Chicago Manual of Style (16^th Edition):

Mattingly, Brendan Christopher. “EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/7832.

MLA Handbook (7^th Edition):

Mattingly, Brendan Christopher. “EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal.” 2011. Web. 28 Jan 2021.

Vancouver:

Mattingly BC. EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/7832.

Council of Science Editors:

Mattingly BC. EXC-5 Controls Intracellular Trafficking in Order to Maintain the Apical Structure of the C. elegans Excretory Canal. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/7832

University of Kansas

7. Mi, Zhen. REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS.

Degree: PhD, Pharmacology & Toxicology, 2015, University of Kansas

URL: http://hdl.handle.net/1808/21731

► Dendritic spines are small membranous protrusions from the dendrites of neuron, which are thought to serve as basic units of synaptic transmission, learning and memory.… (more)

▼ Dendritic spines are small membranous protrusions from the dendrites of neuron, which are thought to serve as basic units of synaptic transmission, learning and memory. Disruptions in dendritic spine shape, size or number are associated with many brain diseases. Mounting evidence suggests that serotonin 2A (5-HT2A) receptors, the most abundant serotonin receptors in the prefrontal cortex, are involved in the regulation of dendritic spines. It has been suggested that both agonists (such as DOI) and antagonists (such as atypical antipsychotics) of 5-HT2A receptors can modulate different aspects of dendritic spines, however, the underlying mechanisms still remains unknown. In this dissertation, mechanisms underlying regulation of dendritic spines by both agonists and antagonists of 5-HT2A receptors are extensively studied and presented. I hypothesize that 5-HT2A receptor agonist regulate dendritic spines via transglutaminase- (TGase) catalyzed serotonylation of small G protein of the Rho family, whereas atypical antipsychotics change dendritic spines via activation of the Janus Kinase 2 (JAK2) signaling pathway. In the first study, the mechanisms and the functional consequences of 5-HT2A receptor-induced serotonylation of small G proteins of the Rho family were investigated in primary rat cortical neurons. Stimulation of 5-HT2A/2C receptors caused TGase-mediated transamidation and activation of Rac1 and Cdc42, but not RhoA, in both A1A1v cells and rat primary cortical culture. DOI-induced Rac1 transamidation occurs at Q61 in A1A1v cells, as demonstrated by site-directed mutagenesis at Q61 of Rac1. Furthermore, our findings were extended from 5-HT2A/2C receptors to another Gαq/11-coupled receptor, muscarinic acetylcholine receptors. In addition, stimulation of 5-HT2A/2C receptors by DOI leads to a transient dendritic spine enlargement, which was blocked by TGase inhibitor cystamine, suggesting 5-HT2A/2C receptors-induced transamidation of Rac1 and Cdc42 is involved in the regulation of dendritic spines by 5-HT2A/2C receptors. In the second study, to study the role of JAK2/ STAT pathway in the regulation of dendritic spines, Sprague-Dawley rats were pretreated with the JAK2 inhibitor AG490 or vehicle, followed by administration with olanzapine or vehicle daily for seven days. Microarray analysis of prefrontal cortices showed that 205 genes were significantly changed by AG490, olanzapine or the combination of both drugs compared to the controls. 92 of the 205 genes are changed by olanzapine via JAK2 signaling pathway. These genes are involved in the etiology of schizophrenia, neuronal signal transduction, neuronal growth factor, metabolism and energy, and synaptic plasticity. mRNA and protein levels of these genes were verified using real-time qPCR, western blot and the enzyme-linked immunosorbent assay (ELISA). Investigation on dendritic morphology shows that treatment with olanzapine induced a maturation in dendritic spines via both JAK2 dependent and independent pathways. Advisors/Committee Members: Muma, Nancy A (advisor), Muma, Nancy A (cmtemember), Bortolato, Marco (cmtemember), Wang, Xinkun (cmtemember), Lundquist, Erik A (cmtemember), Li, Qian (cmtemember).

Subjects/Keywords: Neurosciences; Molecular biology; atypical antipsychotics; dendritic spines; JAK/STAT; serotonin 2A receptor; small G protein of the Rho family; transamidation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mi, Z. (2015). REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/21731

Chicago Manual of Style (16^th Edition):

Mi, Zhen. “REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS.” 2015. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/21731.

MLA Handbook (7^th Edition):

Mi, Zhen. “REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS.” 2015. Web. 28 Jan 2021.

Vancouver:

Mi Z. REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS. [Internet] [Doctoral dissertation]. University of Kansas; 2015. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/21731.

Council of Science Editors:

Mi Z. REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS. [Doctoral Dissertation]. University of Kansas; 2015. Available from: http://hdl.handle.net/1808/21731

University of Kansas

8. Swartzlander, Denny. Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia.

Degree: PhD, Molecular Biosciences, 2016, University of Kansas

URL: http://hdl.handle.net/1808/24192

► Reproductive isolation maintains species barriers and can cause population divergence. Pre-mating isolation prevents courtship between species and can be caused by changes in gene expression… (more)

▼ Reproductive isolation maintains species barriers and can cause population divergence. Pre-mating isolation prevents courtship between species and can be caused by changes in gene expression resulting in sex- and species-specific phenotypes. In Drosophila, courtship is heavily influenced by the production and reception of cuticular hydrocarbons (CHCs), which act as pheromones that elicit or repel courtship from a potential mate. Differences in expression of genes involved in CHC biosynthesis between species can produce different types of CHCs, resulting in species-specific CHC profiles. Differential CHC profiles can result in courtship barriers between species. Drosophila simulans and D. sechellia are asymmetrically reproductively isolated from each other in part because of differential production of CHCs. D. simulans males and females produce 7-tricosene (7-T) whereas D. sechellia males produce 7-T and D. sechellia females produce 7,11-heptacosadiene (7,11-HD). 7,11-HD acts as an anti-aphrodisiac to D. simulans males, which only court D. simulans females. D. sechellia males court both D. simulans and D. sechellia females. Thus reproductive isolation occurs between D. simulans males and D. sechellia females. Genomic regions containing desatF and eloF, among other genes, have been identified by quantitative trait locus (QTL) studies as potentially contributing to production of the D. sechellia pheromone 7,11-HD. In this study I tested the hypothesis that desatF and eloF influence reproductive isolation between D. simulans and D. sechellia. In the first set of experiments, using gene expression analysis, I measured the mRNA production of desatF and eloF, as well as other desaturases and elongases associated with QTL affecting CHC differences between D. simulans and D. sechellia. Both eloF and desatF were expressed only in females of D. sechellia. The other genes had variable expression patterns that did not suggest involvement in sex-specific CHC production. Using allele-specific qPCR in D. simulans/D. sechellia hybrids, I found that only the D. sechellia alleles of desatF and eloF are expressed, implying that desatF and eloF expression differences between females of D. simulans and D. sechellia are likely caused by a cis-regulatory change. To further examine the differences in desatF and eloF expression, in the second set of experiments I introgressed the D. simulans alleles of desatF and eloF into a D. sechellia background. Introgression lines did not express the D. simulans desatF and/or eloF alleles. To determine the effect of desatF and eloF expression on courtship, I measured the courtship behavior of D. simulans and D. sechellia males toward the introgression lines. The time required for a male to start courting did not depend upon the target females, whether it was an introgression line, conspecific or heterospecific. In contrast, the courtship effort of males differed by target female. Male D. simulans courted all introgression lines, and some lines received significantly more courtship than D. sechellia… Advisors/Committee Members: Gleason, Jennifer M (advisor), Macdonald, Stuart J (cmtemember), Lundquist, Erik A (cmtemember), Ward, Robert E (cmtemember), Blumenstiel, Justin P (cmtemember).

Subjects/Keywords: Genetics; Evolution & development; Molecular biology; cuticular hydrocarbons; drosophila courtship; gene expression; pheromones; reproductive isolation

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APA (6^th Edition):

Swartzlander, D. (2016). Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/24192

Chicago Manual of Style (16^th Edition):

Swartzlander, Denny. “Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia.” 2016. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/24192.

MLA Handbook (7^th Edition):

Swartzlander, Denny. “Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia.” 2016. Web. 28 Jan 2021.

Vancouver:

Swartzlander D. Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia. [Internet] [Doctoral dissertation]. University of Kansas; 2016. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/24192.

Council of Science Editors:

Swartzlander D. Gene Expression and Introgression of Two Genes Implicated in Behavioral Reproductive Isolation between Drosophila simulans and D. sechellia. [Doctoral Dissertation]. University of Kansas; 2016. Available from: http://hdl.handle.net/1808/24192

University of Kansas

9. Eldredge, Ken Taro. Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution.

Degree: PhD, Ecology & Evolutionary Biology, 2017, University of Kansas

URL: http://hdl.handle.net/1808/26005

► Aleocharinae is the largest subfamily in the largest family of beetles, the rove beetles. The subfamily has at least 61,575 species divided into 63 tribes,… (more)

▼ Aleocharinae is the largest subfamily in the largest family of beetles, the rove beetles. The subfamily has at least 61,575 species divided into 63 tribes, and is arguably one of the most taxonomically and ecologically diverse lineage of extant metazoans. Among the Aleocharinae, 99% of the taxonomic diversity and ecological diversity belongs to a lineage characterized by the presence of a tergal gland, the gland-clade, which ancestrally functions as a defensive weapon. Subsequent reprogramming of glandular chemistry has taken place, particularly in lineages that have evolved to live with social insects, or ants and termites in particular. In addition, many of these symbiotic groups have evolved additional glands throughout their bodies, demonstrating the inherently adaptive nature of glands in the aleocharine body plan. Therefore, it is possible that the tergal gland was a key innovation that fueled aleocharine diversification. However, very little is known about the early evolution of no-gland lineages, in particular, what anatomical changes may have accompanied the evolutionary origin of the tergal gland. Molecular phylogenetic analyses of the tachyporine-group and early diverging Aleocharinae were conducted. The tachyporine-group was not recovered as a monophyletic group. While Habrocerinae, Olisthaerinae, Phloeocharinae, and Trichophyinae were recovered forming a clade, Aleocharinae and Tachyporinae nested outside of this group. Tachyporinae was recovered polyphyletic and Tachyporini sister to Aleocharinae, supported by the shared presence of a hind coxal lamella. Aleocharinae was recovered monophyletic with no-gland tribes forming an early diverging grade leading up to a monophyletic gland-clade. The unique multisegmented paramere is the most characteristic and an unambiguous synapomorphy for Aleocharinae. The gland-clade was recovered non-monophyletic due to the exclusion of Hypocyphtini, potentially implying an independent evolution of the tergal gland in this tribe. The long presumed sister-group relationship between Gymnusini and Deinopsini was not recovered, despite many shared anatomical similarities. Although similarities between Deinopsini and Gymnusini may be the result of convergence, I hypothesize that their overall anatomy is plesiomorphic for the subfamily. I further hypothesize that the tergal gland acting as a key innovation was contingent on the abandonment of the ancestrally limuloid bodyform at the common ancestor of the gland- clade, and combined with increased sexual selection, fueled gland-clade diversification. The morphology of Aleocharinae was reevaluated in light of the results obtained from phylogenetic analyses of the tachyporine-group and no-gland aleocharine tribes. A total of 328 anatomical terms are recognized in this study, with 77 or 23% being novel. Plotting number of terms by character system revealed that the majority of the variation belongs to the mouthparts (52%), followed by a far second male genitalia (19%). Based on the distribution of anatomical terms, it is likely that… Advisors/Committee Members: Engel, Michael S. (advisor), Thayer, Margaret K. (cmtemember), Cartwright, Paulyn (cmtemember), Holder, Mark T. (cmtemember), Lundquist, Erik A. (cmtemember).

Subjects/Keywords: Entomology; Evolution & development; Systematic biology; Aleocharinae; Ecology; Evolution; Morphology; Phylogeny; Staphylinidae

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Eldredge, K. T. (2017). Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/26005

Chicago Manual of Style (16^th Edition):

Eldredge, Ken Taro. “Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution.” 2017. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/26005.

MLA Handbook (7^th Edition):

Eldredge, Ken Taro. “Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution.” 2017. Web. 28 Jan 2021.

Vancouver:

Eldredge KT. Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution. [Internet] [Doctoral dissertation]. University of Kansas; 2017. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/26005.

Council of Science Editors:

Eldredge KT. Morphological and Molecular Insights into Aleocharine Rove Beetle Evolution. [Doctoral Dissertation]. University of Kansas; 2017. Available from: http://hdl.handle.net/1808/26005

University of Kansas

10. Wang, Suya. Retinoic Acid Plays Critical Roles in the Late Development of the Heart.

Degree: PhD, Pharmacology & Toxicology, 2017, University of Kansas

URL: http://hdl.handle.net/1808/27339

► Vitamin A, via its active metabolite retinoic acid (RA), actively participates in many biological processes including cardiogenesis. Yet RA was found to be highly teratogenic… (more)

▼ Vitamin A, via its active metabolite retinoic acid (RA), actively participates in many biological processes including cardiogenesis. Yet RA was found to be highly teratogenic as both excess and deficiency of this critical morphogen result in congenital heart defects. Studies presented here aims to gain insight in mechanisms regulating RA metabolism during embryogenesis and enrich our knowledge of the critical roles of RA during late heart development. Previously, our lab reported that a short-chain dehydrogenase/reductase, i.e. DHRS3, is required for preventing excessive accumulation of RA and thus safeguarding mouse embryogenesis during mid-gestation. The current study expanded the investigation and studied the physiological importance of DHRS3 in RA metabolism at multiple embryonic stages. Consistent with the elevated RA synthesis and signaling at E14.5, genetic ablation of Dhrs3 results in an expansion of RA signaling at E10.5 and E12.5 globally; as well as in the fetal hearts at E10.5, 12.5 and 13.5. Dhrs3-null mutants display a spectrum of congenital defects, including defects in the heart, skeleton and cranial nerves, which collectively result in mid-gestational lethality in Dhrs3-/- embryos. Reduction of maternal intake of vitamin A successfully rescued the Dhrs3-/- fetuses and allows them to survive into full-size adults with normal growth rate. These data jointly demonstrated the indispensability of DHRS3 in reducing the accumulation of RA in various developmental stages and in the formation of fetal organs. With the advancement of knowledge in RA metabolism gained in the first part of this dissertation, the critical roles of RA in cardiogenesis was further explored in the current work. During late cardiogenic stages, the major source of RA is the epicardium. Epicardium contributes greatly to the formation of coronary vessels and the myocardium via 1) giving rise to migratory epicardial cells that differentiate into perivascular cells, and 2) secreting cardiogenic factors. This dissertation employed multiple in vivo and in vitro models to determine the influence of RA on epicardial behaviors and the subsequent epicardial-regulated cardiogenic events. In vitro studies demonstrated that inhibition of RA synthesis in epicardial cell disrupted cytoskeletal reorganization and preserved epithelial characteristics, which resulted in a reduction of migration of epicardial cells. On the contrary, addition of RAR agonist to activate RA signaling strongly induced remodeling of cytoskeleton represented by the formation of stress fibers as well as filopodia marked by polymerized F-actin. RA signaling also abolished the membranous distribution of epithelial markers and induces expression of numerous metalloproteases to pave the way for cell migration. Data from in vivo models showed consistent observation in the regulation of epicardial migration by RA: excess RA in Dhrs3-/- embryos enhances the intramyocardial invasion of epicardial cells whereas deficiency of RA largely retained epicardial cells in the intact epicardium… Advisors/Committee Members: Shi, Honglian (advisor), Moise, Alexander R. (cmtemember), Yan, Shidu (cmtemember), Azuma, Mizuki (cmtemember), Lundquist, Erik A. (cmtemember).

Subjects/Keywords: Developmental biology; cardiogenesis; coronary vessel formation; epithelial to mesenchymal transition; retinoic acid

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, S. (2017). Retinoic Acid Plays Critical Roles in the Late Development of the Heart. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/27339

Chicago Manual of Style (16^th Edition):

Wang, Suya. “Retinoic Acid Plays Critical Roles in the Late Development of the Heart.” 2017. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/27339.

MLA Handbook (7^th Edition):

Wang, Suya. “Retinoic Acid Plays Critical Roles in the Late Development of the Heart.” 2017. Web. 28 Jan 2021.

Vancouver:

Wang S. Retinoic Acid Plays Critical Roles in the Late Development of the Heart. [Internet] [Doctoral dissertation]. University of Kansas; 2017. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/27339.

Council of Science Editors:

Wang S. Retinoic Acid Plays Critical Roles in the Late Development of the Heart. [Doctoral Dissertation]. University of Kansas; 2017. Available from: http://hdl.handle.net/1808/27339

University of Kansas

11. Zhang, Xinyue. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.

Degree: PhD, Pharmacology & Toxicology, 2018, University of Kansas

URL: http://hdl.handle.net/1808/27832

► Peripheral neuropathies can be classified into two categories, demyelinating or axonal neuropathy. Demyelinating neuropathies are characterized by damaged myelin but intact axons. Recent evidence suggests… (more)

▼ Peripheral neuropathies can be classified into two categories, demyelinating or axonal neuropathy. Demyelinating neuropathies are characterized by damaged myelin but intact axons. Recent evidence suggests that the leucine zipper transcription factor c-jun is at the center of driving demyelination. c-Jun is required for Schwann cells (SCs) to dedifferentiate after injury, and up-regulation of c-jun has been reported in human neuropathies. It remains to be tested whether c-jun would be a valid target for treating demyelinating neuropathies. Previously, our published work has shown that modulating the expression of heat shock protein 70 (Hsp70) using a novel small molecule drug called KU-32 attenuated the expression of c-jun and the extent of demyelination in SC-dorsal root ganglia (DRG) co-cultures in an Hsp70 dependent manner. To extend these data, this work examined the in vivo effects of modulating molecular chaperones using the next generation novologue KU-596 in two mouse models of demyelinating neuropathies. MPZ-Raf mice are a conditional transgenic mouse line that exhibits a demyelinating neuropathy due to the SC-specific induction of mitogen-activated protein kinase (MAPK) and c-jun induction after tamoxifen (TMX) injections in adult mice. Five days of TMX treatment induced a severe motor deficits starting from day 8 and treating the MPZ-Raf mice with 20 mg/kg of KU-596 every other day reduced c-jun levels in the sciatic nerves. The decrease in c-jun correlated with an improvement in the myelination status of the nerves and motor function. In line with previous findings, the effects of KU-596 were Hsp70-dependent, as MPZ-RAF × Hsp70 knockout (KO) mice did not show improvement following drug treatment. This study provides proof of principal that modulating molecular chaperones would be beneficial in treating demyelinating neuropathies. However, as this model is less relevant to an actual disease, we complemented our study using a model of human X-linked Charcot-Marie-Tooth disease (CMT1X). CMT1X is caused by the mutation of gap junction beta 1 gene (GJB1) that encodes the gap junction protein connexin 32 (Cx32). Recent evidence suggests an elevated c-jun expression is associated with the disease. Since c-jun could promote demyelination, targeting c-jun using KU-596 could provide a potential therapeutic strategy to treat CMT1X. The pathology of Cx32 deficient (Cx32def) mice occurs in two stages where young mice develop a pre-demyelinating axonopathy, which progresses to a more severe demyelinating neuropathy in older mice. We show that in young mice that exhibit a pre-demyelinating axonopathy, one-month of KU-596 treatment decreased c-jun expression and improved motor nerve conduction velocity (MNCV) and compound muscle action potential (CMAP). In older Cx32def mice that developed a demyelinating neuropathy, 3 months of KU-596 treatment decreased c-jun expression and improved grip strength, MNCV and CMAP. Hsp70 is required for drug efficacy as neither young nor old Cx32def × Hsp70 KO mice showed improvement… Advisors/Committee Members: Dobrowsky, Rick T. (advisor), Lundquist, Erik A. (cmtemember), Shi, Honglian (cmtemember), Wright, Douglas E. (cmtemember), Zhao, Liqin (cmtemember).

Subjects/Keywords: Pharmacology; c-jun; Demyelination; Heat shock protein 70 (Hsp70); Heat shock protein 90 (Hsp90); neuropathy; X-linked Charcot-Marie-Tooth disease (CMT1X)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, X. (2018). Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/27832

Chicago Manual of Style (16^th Edition):

Zhang, Xinyue. “Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.” 2018. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/27832.

MLA Handbook (7^th Edition):

Zhang, Xinyue. “Modulating Molecular Chaperones to Treat Demyelinating Neuropathies.” 2018. Web. 28 Jan 2021.

Vancouver:

Zhang X. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. [Internet] [Doctoral dissertation]. University of Kansas; 2018. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/27832.

Council of Science Editors:

Zhang X. Modulating Molecular Chaperones to Treat Demyelinating Neuropathies. [Doctoral Dissertation]. University of Kansas; 2018. Available from: http://hdl.handle.net/1808/27832

12. Xu, Chenshu. REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR.

Degree: PhD, Pharmacology & Toxicology, 2011, University of Kansas

URL: http://hdl.handle.net/1808/9708

► Liver-enriched nuclear receptor (NR) proteins regulate the expression and activity of several pivotal hepatic biochemical pathways including the uptake, metabolism and excretion of cholesterol, bile… (more)

▼ Liver-enriched nuclear receptor (NR) proteins regulate the expression and activity of several pivotal hepatic biochemical pathways including the uptake, metabolism and excretion of cholesterol, bile acids, glucose, and xenobiotic compounds from the body. The pregnane x receptor (PXR, NR1I2) was first identified in 1998 as a member of the NR superfamily. Over the past decade, it has been well established that PXR functions as a master-regulator of xenobiotic- and drug-inducible expression and activity of numerous genes that encode key members of the phase I and phase II metabolic enzymes, as well as several membrane transporter proteins. In this way, activation of PXR serves as the principal defense mechanism defending the body from toxic insult. Similarly, the PXR protein also forms the molecular basis of an important class of drug-drug interactions in the clinical setting. Moreover, ligand-activated PXR negatively regulates inflammatory processes in both liver and intestine. An integrated model is emerging to reveal a key role for the post-translational modification of PXR in the selective suppression of gene expression, and is opening the door to the study of completely new modes of PXR-mediated gene regulation. This dissertation contributes mainly to two key areas of PXR research: (1) Identification a novel PXR target gene- carboxylesterase 6 (Ces6); (2) a study of the SUMOylation and ubiquitination of PXR protein. The results presented in this dissertation were primarily obtained from mouse and cell-culture systems. Data presented here reveal that activation of the inflammatory response modulates the SUMOylation and ubiquitination status of ligand-bound PXR protein. The SUMOylation and ubiquitination of the PXR protein functions to feedback-repress the inflammatory and xenobiotic responses, respectively. Taken together, the data represent a likely mechanism and provides initial molecular details for the connection between the PXR signaling pathway and inflammation. Studies on post-translational modification of PXR indicate how this protein is converted from a positive regulator in drug metabolism into a transcriptional repressor in inflammatory response. Finally, detailed protocols for purification of mammalian proteins necessary to perform in vitro SUMOylation reactions are presented. Taken together, the work presented in this dissertation contributes to understanding the interface between PXR, drug metabolism, and inflammation, which is expected to produce new opportunities for the development of novel therapeutic strategies. Advisors/Committee Members: Staudinger, Jeff L. (advisor), Dobrowsky, Rick T (cmtemember), Shi, Honglian (cmtemember), Moise, Alex (cmtemember), Lundquist, Erik A. (cmtemember).

Subjects/Keywords: Pharmacology; Toxicology; Carboxylesterase; Constitutive androstane receptor; Inflammation; Pregnane x receptor; Sumoylation

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APA (6^th Edition):

Xu, C. (2011). REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/9708

Chicago Manual of Style (16^th Edition):

Xu, Chenshu. “REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/9708.

MLA Handbook (7^th Edition):

Xu, Chenshu. “REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR.” 2011. Web. 28 Jan 2021.

Vancouver:

Xu C. REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/9708.

Council of Science Editors:

Xu C. REGULATION OF DRUG METABOLISM AND INFLAMMATION BY PREGNANE X RECEPTOR. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/9708

University of Kansas

13. Demarco, Rafael Senos. AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE.

Degree: PhD, Molecular Biosciences, 2011, University of Kansas

URL: http://hdl.handle.net/1808/7696

► The molecular mechanisms leading to axonal guidance are vital for the proper wiring of the nervous system. Many psychiatric disorders may arise from the improper… (more)

▼ The molecular mechanisms leading to axonal guidance are vital for the proper wiring of the nervous system. Many psychiatric disorders may arise from the improper development of the brain. If an axon does not form, or is extended to a place where it is not supposed to be, proper synapses will not form and communication between neurons and neighbor cells will be affected. An axon is extended after the migration of the growth cone. Filopodia and lamellipodia are extended from the growth cone in order to sense the environment for guidance cues. Once signaled, the growth cone migrates to its final target and the axon is developed. A class of proteins called the Rac GTPases is essential for the process of axon pathfinding. In the model nematode Caenorhabditis elegans, MIG-2/RhoG and CED-10/Rac1 are the two redundant Rac GTPases involved in growth cone migration. The main role of Rac GTPases in axon guidance is due to its control over the actin cytoskeleton. The actin-binding UNC-115/abLIM acts downstream of CED-10/Rac1 in axon pathfinding. In Chapters II and III, I describe how Rac signaling activates UNC-115/abLIM. I propose that the scaffolding protein RACK-1 recruits UNC-115/abLIM to the plasma membrane and brings other molecules, such as PKC, for its modulation. Rac GTPases switch between an inactive, GDP-bound form, to an active, GTP-bound form. Activation can be aided by guanine-nucleotide exchange factors (GEFs), and inactivation is enhanced by GTPase activating proteins (GAPs). UNC-73/Trio is a GEF that acts with both MIG-2/RhoG and CED-10/Rac1 in axon guidance. Nevertheless, mutations that disrupt the Rac GEF activity of UNC-73/Trio do not affect axon pathfinding to the same levels as the abolishment of Rac activity seen in the double mutant of mig-2 and ced-10. Along with other evidence, this suggested that there were other molecules involved in the control of Rac GTPases in this process. I performed a candidate-based genetic screen in the C. elegans genome in order to find other DH-containing GEFs that could potentially interact with MIG-2/RhoG and CED-10/Rac1. In Chapter IV, I show that the Rac GEF TIAM-1 acts upstream of MIG-2/RhoG and CED-10/Rac1 as a linker between these GTPases and CDC-42, another member of the Rho subfamily of small GTPases. Moreover, previous studies have implicated Rac GTPases, but not UNC-73/Trio, in the UNC-6/Netrin attractive signaling system. I show that TIAM-1 is the GEF recruited for this system. In Chapter V I show that other GEFs are also involved in this process. The Rac GEF PIX-1/βPIX, and two CDC-42 GEFs, UIG-1/Clg and EXC-5/FGD1, are also involved in the control of Rac GTPases during axon development. In summary, my work has shown how Rac GTPases control the activity of the actin-binding protein UNC-115/abLIM, and how Rac GTPases themselves are controlled during the process of axon guidance. Advisors/Committee Members: Lundquist, Erik A (advisor), MacDonald, Stuart J. (cmtemember), Ackley, Brian (cmtemember), Corbin, Victoria L. (cmtemember), Neufeld, Kristi L. (cmtemember), Timmons, Lisa (cmtemember), Gleason, Jennifer M. (cmtemember).

Subjects/Keywords: Neurosciences; Genetics; Actin cytoskeleton; Gef; Rac gtpase; Rack-1; Tiam-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Demarco, R. S. (2011). AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7696

Chicago Manual of Style (16^th Edition):

Demarco, Rafael Senos. “AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE.” 2011. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/7696.

MLA Handbook (7^th Edition):

Demarco, Rafael Senos. “AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE.” 2011. Web. 28 Jan 2021.

Vancouver:

Demarco RS. AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE. [Internet] [Doctoral dissertation]. University of Kansas; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/7696.

Council of Science Editors:

Demarco RS. AN AXON'S JOURNEY TO FIND ITS PATH: IN VIVO CHARACTERIZATION OF THE MODULATORS AND EFFECTORS OF THE RAC GTPASE SIGNALING PATHWAY INVOLVED IN AXON GUIDANCE. [Doctoral Dissertation]. University of Kansas; 2011. Available from: http://hdl.handle.net/1808/7696

14. Josephson, Matthew P. New roles for Hox and Wnt in Cell Migration.

Degree: PhD, Molecular Biosciences, 2016, University of Kansas

URL: http://hdl.handle.net/1808/22402

► Neuron migration is a critical process during central nervous system development. In the dissertation below I report new roles for established genes such as Wnt… (more)

▼ Neuron migration is a critical process during central nervous system development. In the dissertation below I report new roles for established genes such as Wnt and Hox, and describe roles for several new genes in neuron migration. To study migrating neurons I use the model organism nematode worm Caenorhabditis elegans. With only 302 neurons, C. elegans is an excellent model to examine migration of individual neurons. The QR and QL neuroblasts are two bilaterally symmetric neural progenitor cells born in the posterior region of the worm. Although born in the same area, these cells undergo opposite directions of migration. QR migrates anteriorly, and QL migrates posteriorly. In QL, detection of extracellular EGL-20/Wnt results in trasncription of mab-5/Antennapedia/Hox through canonical Wnt signalling. MAB-5 is a posterior migration determinant of the QL lineage, and expression of mab-5 is necessary and sufficient for posterior migration. lin-39/Sex combs reduced/Hox is activated through unknown mechanisms in QR and promotes anterior migration of that lineage. lin-39 and mab-5 are well studied genes than have been implicated in cell-autonomous control of Q migrations. After an introduction to Q cell migration in chapter I, chapter II describes new roles for Hox gene in Q descendant migration that may change the way we think about how Hox genes work. I show that lin-39, mab-5 and a third Hox gene egl-5/Abdominal-B/Hox act in parallel to promote migration of the Q cells, and in their absence almost no migration occurs. This in contrast to the typical opposing roles of Hox genes whereby lin-39 promotes anterior migration of QR lineage, and mab-5 promotes posterior migration of the QL lineage. I also find that mab-5, and egl-5 are able to promote Q migration through their expression in posterior body wall muscles, a non-autonomous role in migration. Again this shifts how Hox genes should be considered, as they are often thought to act solely as autonomous drivers of cell fate and to have opposing roles in differentiation. As a Hox factor mab-5 regulates many genes, but few mab-5 targets have been identified. Results in this dissertation show that mab-5 may regulate the secreted F-spondin homolog spon-1 to control migration. I demonstrate that the spon-1 promoter can be driven by MAB-5 in the body wall muscles, and that spon-1 is important in Q cell direction and extent of migration. Chapter III presents new roles for egl-20/Wnt and mab-5/Hox in inhibiting anterior migration. Detailed analysis of the timing of Q descendant migration reveals that egl-20/Wnt can act in two steps to inhibit anterior migration and promote posterior migration of the QL linage. (i) Through an acute non-canonical Wnt mechanism EGL-20 inhibits anterior migration, and (ii) later, through canonical Wnt pathway activates transcription of mab-5 which can further inhibit anterior migration and promote further migration of the QL lineage. The first characterization of the C. elegans Neurofibromatosis Type II(NF2)/Merlin homolog nfm-1 is detailed in… Advisors/Committee Members: Lundquist, Erik A (advisor), Ackley, Brian (cmtemember), Macdonald, Stuart (cmtemember), Ward, Rob (cmtemember), Michaelis, Eli (cmtemember).

Subjects/Keywords: Developmental biology; Genetics; Molecular biology; EGL-20; Hox; MAB-5; migration; SPON-1; Wnt

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APA (6^th Edition):

Josephson, M. P. (2016). New roles for Hox and Wnt in Cell Migration. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/22402

Chicago Manual of Style (16^th Edition):

Josephson, Matthew P. “New roles for Hox and Wnt in Cell Migration.” 2016. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/22402.

MLA Handbook (7^th Edition):

Josephson, Matthew P. “New roles for Hox and Wnt in Cell Migration.” 2016. Web. 28 Jan 2021.

Vancouver:

Josephson MP. New roles for Hox and Wnt in Cell Migration. [Internet] [Doctoral dissertation]. University of Kansas; 2016. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/22402.

Council of Science Editors:

Josephson MP. New roles for Hox and Wnt in Cell Migration. [Doctoral Dissertation]. University of Kansas; 2016. Available from: http://hdl.handle.net/1808/22402

15. Grussendorf, Kelly Ann. Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes.

Degree: PhD, Molecular Biosciences, 2013, University of Kansas

URL: http://hdl.handle.net/1808/12228

► Biological tubes are ubiquitous structures that carry out vital roles. The formation and maintenance of these tubule structures is a fundamental process in most organisms.… (more)

▼ Biological tubes are ubiquitous structures that carry out vital roles. The formation and maintenance of these tubule structures is a fundamental process in most organisms. The goal of this work is to get a better understanding of the molecules required for these processes. The C. elegans excretory canal provides an ideal model for these studies. The family of EXC proteins is required to maintain the tubule shape of the excretory canal. Mutations in the exc genes (EXcretory Canal abnormal) result in the formation of fluid-filled cysts in the lumen of the canal. exc-1 mutants show cysts in the canals that are often located at the ends of the canals. These cysts vary in size and number; from cysts not much wider than normal lumen up to cysts expanded to the entire diameter of the worm. This dissertation describes the work that I carried out to map, clone, and characterize exc-1. EXC-1 is homologous to the family of Immunity-Related GTPases (IRGP) and contains tandem Ras-homology domains. IRGPs make up a large family of proteins, with many of the members involved in the clearance of infectious pathogens, by assisting in autophagy. EXC-1 contains highest homology to the member of IRGPs, IRGC, of which very little is known. The family of IRGPs, and EXC-1's homology to this family and the Ras superfamily is described here. exc-1 is expressed within the excretory canal and the amphid sheath cells, a glial structure that ensheaths the amphid neuron sensory endings. exc-1 mutants exhibit occasional, abnormal formation of cyst-like structures along the process of the amphid sheath, but does not disrupt the formation of the amphid channel, the passageway for exposure of amphid dendrites to the outside environment. exc-1 interacts genetically with exc-5 (Faciogenital dysplasia protein 4 homologue) and exc-9 (Cysteine Rich Intestinal Protein homologue) in a pathway of exc-9 → exc-1 → exc-5. Binding assays show that EXC-1 and EXC-9 bind when EXC-1 is in its wild-type or GTP-bound, active, form. This work also describes the studies carried out to identify the subcellular role of EXC-1 within the canal. With a group of subcellular markers it has been identified that EXC-1 is required for proper trafficking of material from early endosomes to recycling endosome within the excretory canal, similar to EXC-5. This work indicates that EXC-1 and EXC-9 binding is required for downstream activation of EXC-5 for proper trafficking within the canal and maintenance of tubule shape. Advisors/Committee Members: Buechner, Matthew J. (advisor), MacDonald, Stuart J. (cmtemember), Lundquist, Erik A. (cmtemember), Azuma, Yoshiaki (cmtemember), Smith, Debroah (cmtemember).

Subjects/Keywords: Molecular biology; Exc-1; Irgp; Subcellular trafficking; Tubulogenesis

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APA (6^th Edition):

Grussendorf, K. A. (2013). Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/12228

Chicago Manual of Style (16^th Edition):

Grussendorf, Kelly Ann. “Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes.” 2013. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/12228.

MLA Handbook (7^th Edition):

Grussendorf, Kelly Ann. “Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes.” 2013. Web. 28 Jan 2021.

Vancouver:

Grussendorf KA. Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes. [Internet] [Doctoral dissertation]. University of Kansas; 2013. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/12228.

Council of Science Editors:

Grussendorf KA. Cloning and characterization of EXC-1, an IRGP homologue that controls Intracellular Trafficking and the Maintenance of Shape in Small Biological Tubes. [Doctoral Dissertation]. University of Kansas; 2013. Available from: http://hdl.handle.net/1808/12228

16. Li, Chengyuan. Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination.

Degree: PhD, Pharmacology & Toxicology, 2012, University of Kansas

URL: http://hdl.handle.net/1808/13029

► Abstract Modulating molecular chaperones is emerging as an attractive approach to treat neurodegenerative diseases associated with protein aggregation, diabetic peripheral neuropathy (DPN) and possibly, demyelinating… (more)

Subjects/Keywords: Pharmacology; Neurosciences; Medicine; Demyelination; Diabetic peripheral neuropathy; Hsp70; Hsp90 inhibitor; Neuregulin; Pharmacological treatment

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APA (6^th Edition):

Li, C. (2012). Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/13029

Chicago Manual of Style (16^th Edition):

Li, Chengyuan. “Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination.” 2012. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/13029.

MLA Handbook (7^th Edition):

Li, Chengyuan. “Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination.” 2012. Web. 28 Jan 2021.

Vancouver:

Li C. Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination. [Internet] [Doctoral dissertation]. University of Kansas; 2012. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/13029.

Council of Science Editors:

Li C. Small Molecule Hsp90 Modulator and Neuregulin-induced Peripheral Demyelination. [Doctoral Dissertation]. University of Kansas; 2012. Available from: http://hdl.handle.net/1808/13029

17. Al-Hashimi, Hikmat Imad. exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes.

Degree: PhD, Molecular Biosciences, 2018, University of Kansas

URL: http://hdl.handle.net/1808/27803

► The excretory canals of Caenorhabditis elegans are a model for understanding the maintenance of apical morphology in narrow single-celled tubes. Light and electron microscopy shows… (more)

▼ The excretory canals of Caenorhabditis elegans are a model for understanding the maintenance of apical morphology in narrow single-celled tubes. Light and electron microscopy shows that mutants in exc-2 start to form canals normally, but these swell to develop large fluid-filled cysts that lack a complete terminal web at the apical surface, and accumulate filamentous material in the canal lumen. Here, whole-genome sequencing and gene rescue show that exc-2 encodes intermediate filament protein IFC-2. EXC-2/IFC-2 protein, fluorescently tagged via CRISPR/Cas9, is located at the apical surface of the canals independently of other intermediate filament proteins. EXC-2 is also located in several other tissues, though the tagged isoforms are not seen in the larger intestinal tube. Tagged EXC-2 binds via pulldown to intermediate filament protein IFA-4, which is also shown to line the canal apical surface. Overexpression of either protein results in narrow but shortened canals. These results are consistent with a model whereby three intermediate filaments in the canals, EXC-2, IFA-4, and IFB-1, restrain swelling of narrow tubules in concert with actin filaments that guide the extension and direction of tubule outgrowth, while allowing the tube to bend as the animal moves. Additionally, a focused reverse genomic screen of genes highly expressed in the canals found 21 new genes that significantly affect outgrowth or diameter of the canals. These genes nearly double the number of candidates that regulate canal size. Two genes act as suppressors on a pathway of conserved genes whose products mediate vesicle movement from early to recycling endosomes. The encoded proteins provide new tools for understanding the process of cellular recycling and its role in maintaining the narrow diameter of single-cell tubulogenesis. Advisors/Committee Members: Buechner, Matthew J (advisor), Lundquist, Erik A (cmtemember), Ackley, Brian D (cmtemember), Xu, Liang (cmtemember), Smith, Deborah (cmtemember).

Subjects/Keywords: Genetics; Cellular biology; Molecular biology; C. elegans; Entermediate filamnet; Excretory canal; Tubulogensis

…Sequencing Core at the University of Kansas. Genome data analysis was carried out to identify…

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APA (6^th Edition):

Al-Hashimi, H. I. (2018). exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/27803

Chicago Manual of Style (16^th Edition):

Al-Hashimi, Hikmat Imad. “exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes.” 2018. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/27803.

MLA Handbook (7^th Edition):

Al-Hashimi, Hikmat Imad. “exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes.” 2018. Web. 28 Jan 2021.

Vancouver:

Al-Hashimi HI. exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes. [Internet] [Doctoral dissertation]. University of Kansas; 2018. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/27803.

Council of Science Editors:

Al-Hashimi HI. exc-2, an intermediate filament gene, maintains tubular excretory canals in Caenorhabditis elegans along with ifa-4 and other novel genes. [Doctoral Dissertation]. University of Kansas; 2018. Available from: http://hdl.handle.net/1808/27803

18. Gujar, Mahekta R. NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION.

Degree: PhD, Molecular Biosciences, 2018, University of Kansas

URL: http://hdl.handle.net/1808/28000

► The formation of complex neuronal circuits is crucial for the proper development of the central nervous system. The wiring structure of the nervous system underlies… (more)

▼ The formation of complex neuronal circuits is crucial for the proper development of the central nervous system. The wiring structure of the nervous system underlies its function in sensation and movement, and higher order functions such as learning, memory, and cognition. Disruption of this wiring leads to a number of neurodevelopmental disorders such as developmental disability syndromes, autism, and schizophrenia. Axon guidance is an important aspect in this process of development, as neurons are not born with axons but must actively extend these wires in the developing nervous system to reach their appropriate synaptic targets. The developing axons are led by growth cones, dynamic actin-based structures that sense and respond to extracellular guidance cues that drive the forward motion of the axon. Growth cones contain a dynamic lamellipodial body ringed by filopodial protrusions, both important in guiding the axon to its target destination. Motility and guidance behaviors of the growth cone are regulated by its actin and microtubule (MT) cytoskeleton through the modulatory influence of axon guidance cues, such as UNC-6/Netrin and its guidance receptors UNC-40/DCC and UNC-5 that are present at the leading edge of the growth cone. Netrin is a secreted guidance cue that acts as both an axon attractant and repellant in different receptor contexts. Though the role of Netrin and its receptors in axon pathfinding has been extensively studied, very little is known about how Netrin regulates growth cone behavior and morphology in vivo. Caenorhabditis elegans is a useful system to study axon pathfinding and growth cone development in vivo due to its simple, well-characterized nervous system, transparency and fully sequenced genome. The VD and DD motor neurons reside along the ventral nerve cord of the animal, and their axons normally extend straight dorsally to the dorsal nerve cord to form commissures. Though the DD axons develop during embryogenesis, the VD neurons develop post-embryonically in a well-described and stereotypical manner, making them great candidates to study in vivo growth cone development. After a brief introduction to axon guidance and growth cone morphology in chapter I, chapter II describes a novel role for the C. elegans flavin-containing monooxygenase (FMOs) genes in Netrin-mediated axon guidance and growth cone protrusion. We show that the FMO genes are required for VD/DD motor axon guidance and to restrict growth cone filopodial protrusions downstream of the Netrin receptors UNC-40 and UNC-5 and the Rac GTPases CED-10 and MIG-2 in Netrin-mediated growth cone repulsion. In chapter III we present new roles for UNC-6/Netrin in regulating the polarity and extent of growth cone protrusion through its receptors UNC-40 and UNC-5. We demonstrate that UNC-5 signaling regulates three aspects of growth cone morphology during growth away from UNC-6: (i) inhibition of growth cone protrusion (ii) dorsal leading-edge polarization of F-actin and (ii) restriction of MT entry into the growth cone, possibly via the… Advisors/Committee Members: Lundquist, Erik A (advisor), Ackley, Brian D (cmtemember), Macdonald, Stuart J (cmtemember), Oakley, Berl R (cmtemember), Blumenstiel, Justin P (cmtemember).

Subjects/Keywords: Genetics; Molecular biology; Developmental biology; Axon guidance; F-actin; Growth cone; Microtubules; Polarity; UNC-6/Netrin

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APA (6^th Edition):

Gujar, M. R. (2018). NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/28000

Chicago Manual of Style (16^th Edition):

Gujar, Mahekta R. “NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION.” 2018. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/28000.

MLA Handbook (7^th Edition):

Gujar, Mahekta R. “NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION.” 2018. Web. 28 Jan 2021.

Vancouver:

Gujar MR. NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION. [Internet] [Doctoral dissertation]. University of Kansas; 2018. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/28000.

Council of Science Editors:

Gujar MR. NEW INSIGHTS INTO THE ROLE OF UNC-6/NETRIN IN GROWTH CONE PROTRUSION, POLARITY AND CYTOSKELETAL ORGANIZATION. [Doctoral Dissertation]. University of Kansas; 2018. Available from: http://hdl.handle.net/1808/28000

19. Lan, Lan. The specification and patterning of the Drosophila egg chamber.

Degree: PhD, Molecular Biosciences, 2010, University of Kansas

URL: http://hdl.handle.net/1808/7748

► The generation of cell polarity through the localization of specific mRNAs and proteins to discrete subcellular sites is fundamental to asymmetric cell division, tissue morphogenesis,… (more)

▼ The generation of cell polarity through the localization of specific mRNAs and proteins to discrete subcellular sites is fundamental to asymmetric cell division, tissue morphogenesis, cell migration, and most other developmental processes. While many different localized mRNAs and proteins have been described, the mechanisms by which such molecules become localized are only poorly understood. In the first part of this dissertation, I describe my efforts to unravel the mechanism by which gurken (grk) mRNA becomes localized to the anterodorsal corner of the Drosophila oocyte during mid-oogenesis. Such localization is a key step in the polarization of the mature Drosophila egg and future embryo; defects in grk mRNA localization result in the production of depolarized eggs that give rise to embryos that fail to specify ectodermal, endodermal and mesodermal germ layers and die before hatching. I show, using a transgenic fly assay system, that a conserved sequence element within the grk mRNA, called the GLS (grk localization sequence) is essential for anterodorsal localization. My studies indicate that the GLS functions by mediating the association of grk transcripts with a minus end directed microtubule (MT) motor protein, most probably cytoplasmic dynein. Although MT minus ends are enriched around the nuclear membrane in the oocyte's anterodorsal corner, MT minus ends are also abundant along other regions of the anterior cortex. My data force reconsideration of previous models of grk mRNA localization which propose that grk mRNA transport complexes specifically associate with that subset of MTs whose minus ends are concentrated around the oocyte nucleus. Indeed my data suggest that grk mRNA transport particles associate with all MT populations equally and that anterodorsal localization is brought about through repeated rounds of MT association and anterior transport accompanied by specific trapping of the mRNA at the anterodorsal cortex. The mechanism by which grk becomes trapped is unclear, but probably requires at least one RNA element in addition to the GLS. The second part of the dissertation is focused on the mechanism by which Rab11, a small GTPase best known for its role in trafficking vesicles from recycling endosomes to the plasma membrane, polarizes Drosophila germline stem cells (GSCs). Specifically, I present my characterization of a new Rab11 effector, dRip11 (Drosophila Rab11-family interacting protein). First, I show that dRip11 binds to Rab11 in vitro. Second, I identify a region within the Rab11 protein that is required for binding to dRip11. Third, I show that dRip11 has overlapping expression pattern with Rab11 in GSCs and border cells within the Drosophila ovary. Finally, I describe my attempt to generate and analyze dRip11 mutations. Advisors/Committee Members: Cohen, Robert S. (advisor), Corbin, Victoria L. (cmtemember), Lundquist, Erik A. (cmtemember), Neufeld, Kristi L. (cmtemember), Ward, Robert E. (cmtemember), Ward, Joy (cmtemember).

Subjects/Keywords: Molecular biology; Developmental biology

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APA (6^th Edition):

Lan, L. (2010). The specification and patterning of the Drosophila egg chamber. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7748

Chicago Manual of Style (16^th Edition):

Lan, Lan. “The specification and patterning of the Drosophila egg chamber.” 2010. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/7748.

MLA Handbook (7^th Edition):

Lan, Lan. “The specification and patterning of the Drosophila egg chamber.” 2010. Web. 28 Jan 2021.

Vancouver:

Lan L. The specification and patterning of the Drosophila egg chamber. [Internet] [Doctoral dissertation]. University of Kansas; 2010. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/7748.

Council of Science Editors:

Lan L. The specification and patterning of the Drosophila egg chamber. [Doctoral Dissertation]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/7748

20. Paranjape, Smita Ramesh. Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites.

Degree: PhD, Molecular Biosciences, 2015, University of Kansas

URL: http://hdl.handle.net/1808/21597

► Tau is a microtubule-associated protein that is typically found in the axons of neurons. The aggregation of the tau is a significant event in many… (more)

▼ Tau is a microtubule-associated protein that is typically found in the axons of neurons. The aggregation of the tau is a significant event in many neurodegenerative diseases including Alzheimer's disease. In these disease tau dissociates from microtubules and begins to form toxic insoluble intracellular tau aggregates. The process of conversion of soluble monomeric tau to insoluble aggregates in not well understood. Differential conformational changes in pathological forms of the protein may affect its propensity for aggregation and function. Post translational modifications such as hyperphosphorylation or truncation may induce these conformational changes and alter aggregation and function. The studies described here used in vitro assays to determine how truncation affects tau conformation and how they can alter aggregation and function. This information helps to describe how intrinsic differences due to modifications of tau can manifest themselves in the varying pathologies of tauopathies. Tau aggregation in a common mode of pathogenesis in tauopathies, including Alzheimer's disease. Tau aggregation correlates with dementia and neurodegeneration and is viewed as a potential therapeutic target for AD. Fungi have historically been a good source of medicinally important compounds. We identified secondary metabolites obtained from Aspergillus nidulans as tau aggregation inhibitors. We identified a novel class of tau aggregation inhibitors, azaphilones. Four of the azaphilones inhibited tau aggregation and disassembled pre-formed tau aggregates without inhibiting tau’s ability to polymerize microtubules. Preliminary NMR studies showed that our most potent azaphilone, aza-9 interacts with specific residues of tau protein in a dose dependent fashion. Aza-9 also disassembled tau aggregates formed by aggregation enhancing truncation mutant 1-391 in a dose dependent fashion. Azaphilones are therefore very promising lead compounds for tau aggregation inhibitors, provide a novel scaffold for the same and represent a new class of compounds with tau aggregation inhibitor activity. Advisors/Committee Members: Gamblin, Truman C (advisor), Oakley, Berl (cmtemember), Neufeld, Kristi L (cmtemember), Lundquist, Erik A (cmtemember), Azuma, Yoshiaki (cmtemember), Michaelis, Eli (cmtemember).

Subjects/Keywords: Biochemistry; Molecular biology; Alzheimer's disease; microtubules; tau; tau aggregation inhibitors

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APA (6^th Edition):

Paranjape, S. R. (2015). Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/21597

Chicago Manual of Style (16^th Edition):

Paranjape, Smita Ramesh. “Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites.” 2015. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/21597.

MLA Handbook (7^th Edition):

Paranjape, Smita Ramesh. “Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites.” 2015. Web. 28 Jan 2021.

Vancouver:

Paranjape SR. Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites. [Internet] [Doctoral dissertation]. University of Kansas; 2015. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/21597.

Council of Science Editors:

Paranjape SR. Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites. [Doctoral Dissertation]. University of Kansas; 2015. Available from: http://hdl.handle.net/1808/21597

21. McNeil, Casey Lee. Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster.

Degree: PhD, Molecular Biosciences, 2012, University of Kansas

URL: http://hdl.handle.net/1808/10255

► While it has long been established that populations of animals harbor substantial natural genetic variation for life history traits, an understanding of the location, effect,… (more)

Subjects/Keywords: Genetics; Biology; Drosophila; Genitalia; Qtl; Quantitative genetics; Starvation

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APA (6^th Edition):

McNeil, C. L. (2012). Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/10255

Chicago Manual of Style (16^th Edition):

McNeil, Casey Lee. “Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster.” 2012. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/10255.

MLA Handbook (7^th Edition):

McNeil, Casey Lee. “Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster.” 2012. Web. 28 Jan 2021.

Vancouver:

McNeil CL. Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster. [Internet] [Doctoral dissertation]. University of Kansas; 2012. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/10255.

Council of Science Editors:

McNeil CL. Quantitative Genetic Mapping of Life History Traits in Drosophila melanogaster. [Doctoral Dissertation]. University of Kansas; 2012. Available from: http://hdl.handle.net/1808/10255

22. Huarcaya Najarro, Elvis. The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons.

Degree: PhD, Molecular Biosciences, 2012, University of Kansas

URL: http://hdl.handle.net/1808/10816

► Cadherin proteins are cell adhesion molecules involved in multiple aspects of the development of the nervous system. A subgroup of these proteins, called protocadherin, has… (more)

▼ Cadherin proteins are cell adhesion molecules involved in multiple aspects of the development of the nervous system. A subgroup of these proteins, called protocadherin, has been recently shown to play key roles during the formation of neuronal networks in various animal models. In the model nematode Caenorhabditis elegans, there is only one protocadherin protein, called fmi-1, which has not being fully characterized. Here, I describe the cellular and molecular characterization of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons. Mutant alleles for fmi-1 were originally isolated during a genetic screen looking for genes that regulate synaptic morphology in the D-type GABAergic neurons, which are comprised of DD and VD neurons. In fact, fmi-1 animals display synaptic defects, which include reduced synapse number and aberrant synapse size and morphology, as well as an abnormal accumulation of synaptic vesicles at non-synaptic regions. Electron microscopy data reinforce these observations. Although synaptic defects were present in both the ventral nerve cord (VNC) and the dorsal nerve cord (DNC), it appears that synapses corresponding to the VD neurons are primary affected by fmi-1 mutations. Furthermore, transcriptional analysis suggests that fmi-1 is not present in the VD neurons. In fact, expression of fmi-1 under a promoter that is not active in the VD neurons was able to partially rescue these defects. Therefore, in this cellular context, fmi-1 might be acting cell non-autonomously. Mutations in fmi-1 also cause neurite growth defects in the VD neurons along the anteroposterior (A/P) axis. I have developed a VD-specific marker to visualize and score these defects. VD neurons in fmi-1 animals display two different types of neurite defects. First, an anterior ventral neurite (AVN), which will become the axon, fails to extend fully in the VNC. Second, VD neurons display a posterior ventral neurite (PVN) instead of a normal anterior neurite, which causes commissure patterning defects along the anteroposterior axis (A/P axis). These defects arose during the early development of the VD neurons and they appear not to be caused by defects in cell division or cell fate specification. Fly and vertebrate homologues of fmi-1 can work as part of the planar cell polarity (PCP) pathway. We found that mutations in two core components of the PCP pathway, vang -1 and prkl-1, do not display fmi-1-like defects in the VD neurons. Therefore, fmi-1 might be working independently from the PCP pathway to regulate directional neurite growth in these neurons. Finally, I also describe genetic interactions between fmi-1 and two components of the Wnt pathway, lin-17/frizzled and dsh-1/disheveled. Epistasis analyses suggest that lin-17 and dsh-1 work in a pathway distinct from that of fmi-1 to regulate directional neurite growth in the VD neurons along the A/P axis. In summary, fmi-1 plays multiple roles during the development of the D-type GABAergic neurons. Interestingly, fmi-1 and the Wnt pathway work redundantly… Advisors/Committee Members: Ackley, Brian (advisor), Ackley, Brian (cmtemember), Karanicolas, John (cmtemember), Lundquist, Erik A. (cmtemember), MacDonald, Stuart J. (cmtemember), Kelly, John (cmtemember), Ward, Robert E. (cmtemember).

Subjects/Keywords: Neurosciences; Developmental biology; Axon growth; Cadherin; C. elegans; Flamingo; Fmi-1; Wnt

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APA (6^th Edition):

Huarcaya Najarro, E. (2012). The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/10816

Chicago Manual of Style (16^th Edition):

Huarcaya Najarro, Elvis. “The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons.” 2012. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/10816.

MLA Handbook (7^th Edition):

Huarcaya Najarro, Elvis. “The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons.” 2012. Web. 28 Jan 2021.

Vancouver:

Huarcaya Najarro E. The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons. [Internet] [Doctoral dissertation]. University of Kansas; 2012. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/10816.

Council of Science Editors:

Huarcaya Najarro E. The role of the cadherin fmi-1/flamingo in the development of the D-type GABAergic neurons. [Doctoral Dissertation]. University of Kansas; 2012. Available from: http://hdl.handle.net/1808/10816

University of Kansas

23. Sarthy, Jay Francis. Mechanisms of Telomere Protection and Deprotection in Human Cells.

Degree: PhD, Molecular Biosciences, 2009, University of Kansas

URL: http://hdl.handle.net/1808/6023

► Telomeres, the nucleo-protein complexes at the ends of linear chromosomes, have critical roles in genome stability, cancer, and aging. Early work by B. McClintock and… (more)

▼ Telomeres, the nucleo-protein complexes at the ends of linear chromosomes, have critical roles in genome stability, cancer, and aging. Early work by B. McClintock and H.J. Muller demonstrated that eukaryotic chromosome ends contain specialized structures that prevent recognition and processing by the DNA repair machinery. The importance of these structures is illustrated by studies showing that loss of chromosome end protection results in massive genome instability and cell death. Although Muller and McClintock's initial observations were made several decades ago, little progress has been made in understanding the molecular markers that distinguish naturally occurring chromosome ends from de novo DNA double strand breaks, especially in humans. Using a novel system to specifically target proteins of interest to human telomeres, we have uncovered a role for hRAP1 in protecting telomeres from non-homologous end joining (NHEJ). We find that telomeric DNA containing hRAP1, but not TRF2, is protected from NHEJ in vitro. Furthermore, we show that telomeres containing TRF2 but not hRAP1 can be fused by NHEJ in vivo, and we also demonstrate that targeting hRAP1 to telomeres in vivo, even when TRF2 is not detected, is sufficient to protect telomeres from NHEJ. These results identify hRAP1 as a critical mediator of telomere protection and genome stability in humans. Related to this work, we have also identified a new type of telomere dysfunction associated with semi-conservative replication stress at human telomeres. This new type of telomere dysfunction is telomerase and NHEJ-independent and may require the RecQ helicase WRN for its formation, suggesting that it is related to telomere entanglements observed upon induction of replication stress in fission yeast. The finding that this type of dysfunction is conserved from yeast to man is a testament to the underappreciated role of semi-conservative DNA synthesis in maintaining telomere structure and function. Advisors/Committee Members: Baumann, Peter E. (advisor), Crawford, Michael H. (advisor), Lundquist, Erik A. (cmtemember), Kelly, John (cmtemember), MacDonald, Stuart J. (cmtemember).

Subjects/Keywords: Cell biology; Molecular biology; Biology; Genetics; Cancer; Chromosome dynamics; Genome stability; Telomeres

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sarthy, J. F. (2009). Mechanisms of Telomere Protection and Deprotection in Human Cells. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/6023

Chicago Manual of Style (16^th Edition):

Sarthy, Jay Francis. “Mechanisms of Telomere Protection and Deprotection in Human Cells.” 2009. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/6023.

MLA Handbook (7^th Edition):

Sarthy, Jay Francis. “Mechanisms of Telomere Protection and Deprotection in Human Cells.” 2009. Web. 28 Jan 2021.

Vancouver:

Sarthy JF. Mechanisms of Telomere Protection and Deprotection in Human Cells. [Internet] [Doctoral dissertation]. University of Kansas; 2009. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/6023.

Council of Science Editors:

Sarthy JF. Mechanisms of Telomere Protection and Deprotection in Human Cells. [Doctoral Dissertation]. University of Kansas; 2009. Available from: http://hdl.handle.net/1808/6023

University of Kansas

24. Dyer, Jamie Olivia. Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans.

Degree: PhD, Molecular Biosciences, 2010, University of Kansas

URL: http://hdl.handle.net/1808/6421

► Neuronal migration is essential to the formation of the central nervous system in vertebrates. In Caenorhabditis elegans, a screen was performed previously to identify mutations… (more)

▼ Neuronal migration is essential to the formation of the central nervous system in vertebrates. In Caenorhabditis elegans, a screen was performed previously to identify mutations that affected the migration of the Q neuroblast descendants. One of the mutants isolated from this screen was mig-15. MIG-15, a Nck Interacting Kinase (NIK), is homologous to proteins found in a wide variety of organisms, including Drosophila, mice, and humans, in which NIK kinases have been implicated in cell migration. Interestingly, multiple components of the canonical Wnt signaling pathway had already been found to control the Q cell descendant migrations. Additionally, the MIG-15 homolog in Drosophila, Misshapen had also been found to work with Wnt signaling components in the non-canonical planar cell polarity pathway. To determine how MIG-15 was working to control the migrations of the Q cell descendants, a characterization of the Q neuroblast migration defects was performed. mig-15 mutants were found to affect the Q neuroblasts, along with their descendants as previously described. I carried this work further and found that MIG-15 is required for extension of lamellipodial protrusions, maintenance of the initial polarization directing these initial protrusions, and migration of the Q neuroblasts. Since the Wnt signaling pathway had been implicated in Q cell descendant migration as well, several Wnt signaling mutants were also examined in the Q neuroblasts. This analysis determined that for the Wnt signaling mutants that were observed, there was no effect on early Q neuroblast protrusion extension or migration. Therefore, MIG-15 does not appear to be acting with the Wnt signaling pathway to control Q neuroblast migration. Subsequently, the Q cell descendant migrations of the AQR and PQR neurons were also examined for both mig-15 and Wnt signaling mutants. Double mutants of mig-15 with Wnt signaling mutants resembled mig-15 mutants alone, further suggesting that MIG-15 is not working with the Wnt signaling pathway to control the Q neuroblast lineage migrations. In attempt to elucidate how MIG-15 is controlling the migrations of the Q neuroblasts and descendants, a candidate gene approach was taken to determine other possible proteins that are required for Q neuroblast migration. The C-terminal region of MIG-15 had previously been found to bind to PAT-3, the beta-integrin homolog in C. elegans. Since available mutants in pat-3 are not viable, INA-1/alpha-integrin was examined for defects in Q neuroblast migration. This analysis found that, like MIG-15, INA-1 is required for the extension of polarized protrusions and migration of the Q neuroblasts. Though, INA-1 was not involved in maintenance of polarization as was MIG-15. Another molecule that was examined was ERM-1, the C. elegans homolog of the ezrin, radixin, and moesin (ERM) family of proteins. Previous studies have found that ERM proteins bind to and are phosphorylated by Nck interacting kinases in cell culture. These studies found that removal of ERM-1 from mig-15 mutants… Advisors/Committee Members: Lundquist, Erik A (advisor), Ackley, Brian (cmtemember), Cohen, Robert (cmtemember), Kelly, John (cmtemember), Neufeld, Kristi L. (cmtemember), Timmons, Lisa (cmtemember).

Subjects/Keywords: Developmental biology; Biology; Genetics; Neurosciences; Nck interacting kinase; Nervous system development; Neuronal migration; Rac gtpases

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dyer, J. O. (2010). Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/6421

Chicago Manual of Style (16^th Edition):

Dyer, Jamie Olivia. “Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans.” 2010. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/6421.

MLA Handbook (7^th Edition):

Dyer, Jamie Olivia. “Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans.” 2010. Web. 28 Jan 2021.

Vancouver:

Dyer JO. Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. University of Kansas; 2010. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/6421.

Council of Science Editors:

Dyer JO. Characterization of the roles of the Nck interacting kinase MIG-15 and the Rac GTPases in neuronal migration in Caenorhabditis elegans. [Doctoral Dissertation]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/6421

University of Kansas

25. Zhang, Liang. Genetic Approaches to Study Tissue Morphogenesis in Drosophila.

Degree: PhD, Molecular Biosciences, 2009, University of Kansas

URL: http://hdl.handle.net/1808/5977

► Morphogenesis is defined as the change of body shape over time, the understanding of which is one of the central questions of developmental biology. To… (more)

▼ Morphogenesis is defined as the change of body shape over time, the understanding of which is one of the central questions of developmental biology. To achieve proper overall organ and body shape, morphogenetic movements have to be precisely controlled during development. I have used both genetic and cell biological approaches to study control mechanisms of morphogenesis in the model organism Drosophila melanogaster. Nonmuscle myosin II (myosin hereafter) has well-established roles in generating contractile force on actin filaments during morphogenetic processes. Myosin activation is regulated by phosphorylation of the myosin regulatory light chain (MRCL, encoded by spaghetti squash or sqh in Drosophila) first on Ser-21 and subsequently on Thr-20. These phosphorylation events are positively controlled by a variety of kinases including myosin light chain kinase, Rho kinase, citron kinase, and AMP kinase and are negatively regulated by myosin phosphatase. The activation of myosin is thus highly regulated and is likely developmentally controlled. Therefore in order to monitor the activity of myosin during development, we have generated antibodies against the monophosphorylated (Sqh1P) and diphosphorylated (Sqh2P) forms of Sqh. We first show that the antibodies are highly specific for each phosphorylated form of the protein. We next used these antibodies on wild type Drosophila tissues. Interestingly, Sqh1P predominantly localizes in the adherens junction in imaginal disc cells, whereas Sqh2P locates to the apical domain. Sqh1P and Sqh2P also show distinct patterns of expression in embryos. Sqh1P is expressed nearly ubiquitously and outlines cells consistent with a junctional localization, whereas Sqh2P is strongly expressed in the ventral furrow, the invaginating fore- and hindgut, the invaginating tracheal system, head segments during head involution, and the dorsal most row of epidermal (DME) cells during dorsal closure. These represent tissues that are undergoing extensive cell shape change or cell rearrangements. Sqh2P is localized very apically in these cells, and is noticeably enriched in filopodia emanating from the DME cells during dorsal closure. These antibodies will thus be very useful in monitoring myosin activation for functional studies of morphogenesis. The tracheal system of Drosophila melanogaster has proven to be an excellent model system for studying the development of branched tubular organs. Mechanisms regulating the patterning and initial maturation of the tracheal system have been largely worked out, yet important questions remain regarding how the mature tubes inflate with air at the end of embryogenesis, and how the tracheal system grows in response to the oxygen needs of a developing larva that increases nearly 1000-fold in volume over a four day period. In chapter 2, I describe the cloning and characterization of uninflatable (uif), a gene that encodes a large transmembrane protein containing carbohydrate binding and cell signaling motifs in its extracellular domain. Uif is highly conserved in… Advisors/Committee Members: Ward, Robert E (advisor), Azuma, Yoshiaki (cmtemember), Cohen, Robert (cmtemember), Corbin, Victoria L. (cmtemember), Hileman, Lena C (cmtemember), Lundquist, Erik A. (cmtemember), Richter, Mark (cmtemember).

Subjects/Keywords: Cell biology; Biology; Genetics; Molecular biology; Drosophila; Myosin regulatory light chain; Sqh; Trachea; Uninflatable

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, L. (2009). Genetic Approaches to Study Tissue Morphogenesis in Drosophila. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/5977

Chicago Manual of Style (16^th Edition):

Zhang, Liang. “Genetic Approaches to Study Tissue Morphogenesis in Drosophila.” 2009. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/5977.

MLA Handbook (7^th Edition):

Zhang, Liang. “Genetic Approaches to Study Tissue Morphogenesis in Drosophila.” 2009. Web. 28 Jan 2021.

Vancouver:

Zhang L. Genetic Approaches to Study Tissue Morphogenesis in Drosophila. [Internet] [Doctoral dissertation]. University of Kansas; 2009. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/5977.

Council of Science Editors:

Zhang L. Genetic Approaches to Study Tissue Morphogenesis in Drosophila. [Doctoral Dissertation]. University of Kansas; 2009. Available from: http://hdl.handle.net/1808/5977

University of Kansas

26. Wang, Yang. NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION.

Degree: PhD, Molecular Biosciences, 2009, University of Kansas

URL: http://hdl.handle.net/1808/5459

► Mutations in Adenomatous Polyposis Coli (APC) initiate most colorectal cancers. APC is implicated in regulating cell cycle and the cytoskeleton. I identified topoisomerase IIalpha (topo… (more)

Subjects/Keywords: Cell biology; Molecular biology; Adenomatous polyposis coli; Cell cycle; G2 decatenation checkpoint; Intermediate filament; Lamin b1; Topoisomerase iialpha

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, Y. (2009). NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/5459

Chicago Manual of Style (16^th Edition):

Wang, Yang. “NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION.” 2009. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/5459.

MLA Handbook (7^th Edition):

Wang, Yang. “NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION.” 2009. Web. 28 Jan 2021.

Vancouver:

Wang Y. NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION. [Internet] [Doctoral dissertation]. University of Kansas; 2009. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/5459.

Council of Science Editors:

Wang Y. NUCLEAR FUNCTIONS OF ADENOMATOUS POLYPOSIS COLI: REGULATION OF THE G2-M CELL CYCLE TRANSITION & INTERMEDIATE FILAMENT INTERACTION. [Doctoral Dissertation]. University of Kansas; 2009. Available from: http://hdl.handle.net/1808/5459

University of Kansas

27. Wang, Xiaochen. Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila.

Degree: PhD, Molecular Biosciences, 2010, University of Kansas

URL: http://hdl.handle.net/1808/6402

► Development of Drosophila leg imaginal discs provides an ideal model to study hormone-regulated morphogenesis. During the onset of metamorphosis, a pulse of ecdysone triggers the… (more)

Subjects/Keywords: Biology; Genetics; Developmental biology; Cell biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, X. (2010). Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/6402

Chicago Manual of Style (16^th Edition):

Wang, Xiaochen. “Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila.” 2010. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/6402.

MLA Handbook (7^th Edition):

Wang, Xiaochen. “Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila.” 2010. Web. 28 Jan 2021.

Vancouver:

Wang X. Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila. [Internet] [Doctoral dissertation]. University of Kansas; 2010. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/6402.

Council of Science Editors:

Wang X. Forward and reverse genetic approaches to identify genes involved in leg morphogenesis in Drosophila. [Doctoral Dissertation]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/6402

University of Kansas

28. Tong, Xiangyan. Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure.

Degree: PH.D., Biochemistry & Molecular Biology, 2007, University of Kansas

URL: http://hdl.handle.net/1808/4113

► Forming and maintaining tubular structure is fundamental to organismal development. The excretory canal cell of C.elegans forms a single-cell epithelial tubule, which provides a simple… (more)

▼ Forming and maintaining tubular structure is fundamental to organismal development. The excretory canal cell of C.elegans forms a single-cell epithelial tubule, which provides a simple model for tubular structure study. The EXC proteins regulate maintenance of the apical (lumenal) cytoskeleton of the excretory canal. Loss of exc gene function allows formation of fluid-filled cysts in the excretory canal. exc-9 mutants exhibit short and cystic canals compared to wild-type worms. exc-9 mutants also exhibit tail defects in hermaphrodites and ray defects in male. By SNP mapping, cosmid rescue, and RNAi experiments, we proved that F20D12.5 encodes exc-9. EXC-9 is a homologue of the mammalian intestinal LIM-domain protein CRIP. exc-9 is highly expressed in the canal and tailspike, it is also expressed in some other cells, including UTSE, DTCs, and ALM neurons. Promoter regions important for exc-9 expression were studied. It was found that EXC-9 functions cell-autonomously and the free N-terminus of the protein is required for unextended canal phenotype. Overexpression of exc-9 constructs in an N2 background sometimes causes an "unextended canal" phenotype, in which the canal forms a large cell body filled with lumen with proper diameter, but has no canals along the length of the animal. Since canal extension is sensitive to expression levels of exc-9, injection of the construct also caused unextended canal phenotype in exc-9 mutants. Similar unextended canal phenotype was also found in animals showing high levels of exc-5 expression. I used the unextended canal phenotype to examine epistasis of EXC-9 function with that of other EXC proteins. EXC-9 appears to function upstream of EXC-5 to regulate cytoskeletal formation at the apical surface (possibly via CDC-42); and EXC-9 in turn may depend upon EXC-2 and EXC-4 function. A second well conserved CRIP homologue B0496.7 is highly expressed in multiple valves of C.elegans. It functions similarly to EXC-9 when ectopically expressed in the excretory canal. Expression of the mouse homologue CRIP in the canal failed to rescue exc-9 mutants, but with some modifications, mouse CRIP can function similar as EXC-9. Preliminary data of cloning of exc-2 is reported in this work too. Advisors/Committee Members: Buechner, Matthew J. (advisor), Corbin, Victoria L. (cmtemember), Dentler, William (cmtemember), Lundquist, Erik A. (cmtemember), Timmons, Lisa (cmtemember), Siahaan, Teruna (cmtemember).

Subjects/Keywords: Molecular biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tong, X. (2007). Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/4113

Chicago Manual of Style (16^th Edition):

Tong, Xiangyan. “Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure.” 2007. Doctoral Dissertation, University of Kansas. Accessed January 28, 2021. http://hdl.handle.net/1808/4113.

MLA Handbook (7^th Edition):

Tong, Xiangyan. “Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure.” 2007. Web. 28 Jan 2021.

Vancouver:

Tong X. Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure. [Internet] [Doctoral dissertation]. University of Kansas; 2007. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1808/4113.

Council of Science Editors:

Tong X. Cloning and characterization of exc-9, a Caenorhabditis elegans CRIP homologue that regulates tubular structure. [Doctoral Dissertation]. University of Kansas; 2007. Available from: http://hdl.handle.net/1808/4113

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