+publisher:"University of Kansas" +contributor:("Timmons, Lisa")

University of Kansas

1. 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 21, 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. 21 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 21]. 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

2. Asad, Nadeem. Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans.

Degree: PhD, Molecular Biosciences, 2014, University of Kansas

URL: http://hdl.handle.net/1808/23953

► ABSTRACT Experimentally and/or intrinsically delivered dsRNAs can trigger complex set of mechanisms, acting in multiple cell compartments and tissues throughout developmental time. Several methods are… (more)

▼ ABSTRACT Experimentally and/or intrinsically delivered dsRNAs can trigger complex set of mechanisms, acting in multiple cell compartments and tissues throughout developmental time. Several methods are available for effective delivery of dsRNA to Caenorhabditis elegans, including ingestion-based feeding and soaking methods, injection of dsRNAs, and transgene-mediated transcription of dsRNA in vivo. Feeding is a more commonly used dsRNA-delivery strategy, and the RNAi mechanisms that respond to ingested dsRNAs are better elaborated than the responses to other dsRNA delivery methods. However, cellular mechanisms that are triggered by experimental delivery of dsRNAs also respond to foreign nucleic acids, such as viral and transposon sequences, and these mechanisms are active in the nucleus as well as the cytoplasm. In ingestion-based delivery methods, the dsRNA molecules enter cells from environmental sources, whereas when transgene-based delivery methods are used, dsRNA molecules are generated in the nucleus. Thus, RNAi mechanisms are activated by dsRNAs that enter the cytoplasm from opposite directions. We are investigating RNAi mechanisms with respect to the compartment in which the dsRNAs are generated and the directionality of their movement into the cytoplasm. Our genetics-based studies indicate that, even though intrinsically derived dsRNAs are produced in the nucleus, they depend on cytoplasmic RNAi machinery. In keeping with this model, NRDE-3, an argonaute protein predicted to shuttle silencing RNAs into the nucleus, had no effect on the RNAi responses from RNAi-proficient transgenes configured as extra-chromosomal arrays. (However, modest effects were observed in nrde-3 mutants when the same dsRNA-expressing sequences were present as single-copy-integrants.) We observed a surprising result that transgenes with negligible RNAi activity in wild-type animals gained RNAi activity in nrde-3 as well as hrde-1 mutants, and from these results, we infer that such dsRNA-expressing transgenes are themselves susceptible to NRDE-3 and HRDE-1 mediated silencing, as has previously been observed for mRNA-encoding genes in endogenous chromosomes and transgenes. However, while transgene-based RNAi is independent of MUT-7, MUT-16 is required for an RNAi phenocopy. A variety of factors can influence the RNAi competency of transgenes, including copy number of dsRNA-expressing cassettes, transgene design, temperature, maternal effects, background mutations and inter-compartmental transport. Advisors/Committee Members: Timmons, Lisa D (advisor), Egan, Susan M. (cmtemember), Dentler, William (cmtemember), Buechner, Matthew (cmtemember), Hanson, Paul (cmtemember), Azuma, Mizuki (cmtemember).

Subjects/Keywords: Molecular biology; Developmental biology; Cellular biology; Anti-genome response; C. elegans; Mutators; Nrde-3; RNAi; Transgenes

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

APA (6^th Edition):

Asad, N. (2014). Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/23953

Chicago Manual of Style (16^th Edition):

Asad, Nadeem. “Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans.” 2014. Doctoral Dissertation, University of Kansas. Accessed January 21, 2021. http://hdl.handle.net/1808/23953.

MLA Handbook (7^th Edition):

Asad, Nadeem. “Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans.” 2014. Web. 21 Jan 2021.

Vancouver:

Asad N. Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. University of Kansas; 2014. [cited 2021 Jan 21]. Available from: http://hdl.handle.net/1808/23953.

Council of Science Editors:

Asad N. Cytoplasmic vs. Nuclear RNAi in Caenorhabditis elegans. [Doctoral Dissertation]. University of Kansas; 2014. Available from: http://hdl.handle.net/1808/23953

University of Kansas

3. 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 21, 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. 21 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 21]. 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

4. Lichti-Kaiser, Kristin Nicole. Regulation of the Pregnane X Receptor Signaling Pathway.

Degree: PhD, Pharmacology & Toxicology, 2009, University of Kansas

URL: http://hdl.handle.net/1808/6188

► Liver-enriched nuclear receptors (NRs) collectively function as metabolic and toxicological `sensors' that mediate liver-specific gene-activation in mammals. NR-mediated gene-environment interaction regulates important steps in the… (more)

▼ Liver-enriched nuclear receptors (NRs) collectively function as metabolic and toxicological `sensors' that mediate liver-specific gene-activation in mammals. NR-mediated gene-environment interaction regulates important steps in the hepatic uptake, metabolism and excretion of glucose, fatty acids, lipoproteins, cholesterol, bile acids, and xenobiotics. While it is well-recognized that ligand-binding is the primary mechanism behind activation of NRs, recent research is revealing that multiple signal transduction pathways modulate NR-function in liver. The interface between specific signal transduction pathways and NRs helps to determine their overall responsiveness to various environmental and physiological stimuli. The pregnane x receptor (PXR, NR1I2) was identified in 1998 as a member of the NR superfamily of ligand-activated transcription factors. PXR is activated by a broad range of lipophilic compounds in a species-specific manner. The primary function ascribed to PXR is the homeostatic control of steroids, bile acids, and xenobiotics. This function is mediated through PXR's ability to coordinately activate gene expression and regulate the subsequent activity of phase I and phase II metabolic enzymes, as well as several membrane transporter proteins. While PXR likely evolved primarily to protect the liver from toxic assault, its activation also represents the molecular basis for an important class of drug-drug, herb-drug, and food-drug interactions. While ligand binding is the primary mode of PXR activation, several signal transduction pathways interface with the PXR protein to determine its overall responsiveness to environmental stimuli. Multiple signaling pathways modulate the activity of PXR, likely through direct alteration of the phosphorylation status of the receptor and its protein cofactors. Therefore, specific combinations of ligand binding and cell signaling pathways affect PXR-mediated gene activation and determine the overall biological response. This dissertation contributes to the molecular understanding of the regulation of PXR by novel agonists, cAMP-dependent protein kinase (PKA) signaling, and phosphorylation. The results presented here were primarily obtained from mouse and tissue culture systems. This dissertation identifies Tian Xian, a traditional Chinese herbal anti-cancer remedy, as a novel PXR activator. This evidence suggests that Tian Xian should be used cautiously by cancer patients taking chemotherapy due to its potential to increase the metabolism of co-administered medications. In addition, data presented here show that activation of PKA signaling modulates PXR activity in a species-specific manner. It is further revealed that PXR exists as phospho-protein in vivo and that the activation of PKA signaling modulates the phospho-threonine status of PXR. Finally, the potential phosphorylation sites within the PXR protein are identified. These phosphorylation sites are characterized, using a phosphomimetic and phospho-deficient site-directed mutagenesis based approach, based on their… Advisors/Committee Members: Staudinger, Jeff L. (advisor), Muma, Nancy (cmtemember), Dobrowsky, Rick T (cmtemember), Timmons, Lisa (cmtemember), Carrasco, Gonzalo A. (cmtemember).

Subjects/Keywords: Health sciences; Pharmacology; Cell signaling; Gene expression; Pregnane x receptor

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APA (6^th Edition):

Lichti-Kaiser, K. N. (2009). Regulation of the Pregnane X Receptor Signaling Pathway. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/6188

Chicago Manual of Style (16^th Edition):

Lichti-Kaiser, Kristin Nicole. “Regulation of the Pregnane X Receptor Signaling Pathway.” 2009. Doctoral Dissertation, University of Kansas. Accessed January 21, 2021. http://hdl.handle.net/1808/6188.

MLA Handbook (7^th Edition):

Lichti-Kaiser, Kristin Nicole. “Regulation of the Pregnane X Receptor Signaling Pathway.” 2009. Web. 21 Jan 2021.

Vancouver:

Lichti-Kaiser KN. Regulation of the Pregnane X Receptor Signaling Pathway. [Internet] [Doctoral dissertation]. University of Kansas; 2009. [cited 2021 Jan 21]. Available from: http://hdl.handle.net/1808/6188.

Council of Science Editors:

Lichti-Kaiser KN. Regulation of the Pregnane X Receptor Signaling Pathway. [Doctoral Dissertation]. University of Kansas; 2009. Available from: http://hdl.handle.net/1808/6188

University of Kansas

5. Rivera, Laticia. RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6.

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

URL: http://hdl.handle.net/1808/7747

► The C. elegans rha-1 gene encodes a conserved helicase with ATP-dependent DEAD/H-box and double-stranded RNA binding domains. rha-1 is orthologous to the Drosophila maleless gene(MLE),… (more)

▼ The C. elegans rha-1 gene encodes a conserved helicase with ATP-dependent DEAD/H-box and double-stranded RNA binding domains. rha-1 is orthologous to the Drosophila maleless gene(MLE), an essential component of the dosage compensation machinery that leads to a two-fold increase in transcription of genes located on the single X chromosome of males in comparison to the transcription rate of homologous genes located on an X chromosome in females. The human ortholog, RNA helicase A (RHA), unwinds double-stranded DNA and RNA in a 3' to 5' direction. RHA is a component of several distinct protein complexes, including the RNA-induced silencing complex (RISC), the coding region determinant (CRD)-mediated complex, mRNP granules, and also associates with BRCA1, CREBbp or SMN1 and the RNA polymerase II complex, phosphorylated histones (H2AFX). RHA affects a number of different biological activities, including CRD-mediated mRNA stabilization, RNA splicing, translation, and transcription. It also has been discovered that regulation of RHA is disrupted in many types of cancers. The C. elegans rha-1 gene is expressed in the gonad where it localizes to the nucleus and the cytoplasm and is required for proper development. Defects in rha-1 lead to germline defects, aberrant expression of genes residing in repetitive transgene arrays, and defects in RNAi. ABC transporter proteins have also been implicated to play a role in RNAi in C. elegans. Ten out of the sixty-one ABC transporters are required for efficient RNAi in the germ line; these transporters are called ABCRNAi transporters. All of the ABCRNAi transporter mutants interact genetically with rde-2 (a novel protein) and mut-7 (a protein with homology to RnaseD). One of these ABCRNAi transporter genes is haf-6. The works presented here show that rha-1 mutants also interact genetically with haf-6, with rde-2, and with mut-7 with respect to RNAi defects. By contrast, mutations in rha-1 suppress the transposon mobilization phenotypes observed in haf-6 mutants. It is also observed that an unknown mutation is genetically interacting with rha-1 and haf-6. We are currently investigating roles for rha-1 in proper accumulation of haf-6 and other ABCRNAi transporter mRNAs in an effort to understand the interrelated functions of these proteins in RNAi. Advisors/Committee Members: Timmons, Lisa (advisor), Richter, Mark (cmtemember), Azuma, Mizuki (cmtemember).

Subjects/Keywords: Genetics; Abc transporter; Haf-6; Rnai

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

APA (6^th Edition):

Rivera, L. (2010). RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6. (Masters Thesis). University of Kansas. Retrieved from http://hdl.handle.net/1808/7747

Chicago Manual of Style (16^th Edition):

Rivera, Laticia. “RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6.” 2010. Masters Thesis, University of Kansas. Accessed January 21, 2021. http://hdl.handle.net/1808/7747.

MLA Handbook (7^th Edition):

Rivera, Laticia. “RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6.” 2010. Web. 21 Jan 2021.

Vancouver:

Rivera L. RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6. [Internet] [Masters thesis]. University of Kansas; 2010. [cited 2021 Jan 21]. Available from: http://hdl.handle.net/1808/7747.

Council of Science Editors:

Rivera L. RNA Helicase 1 interacts with an ABCRNAi Transporter: Genetic Interactions with haf-6. [Masters Thesis]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/7747

University of Kansas

6. 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 21, 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. 21 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 21]. 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

7. Marriage, Tara N. Mutation, asexual reproduction and genetic load: A study in three parts.

Degree: PhD, Ecology & Evolutionary Biology, 2009, University of Kansas

URL: http://hdl.handle.net/1808/5949

► My dissertation addresses mutation and complex mating systems (models of mating systems that include outcrossing, selfing, and asexual reproduction) in three distinct chapters. Chapter 2… (more)

Subjects/Keywords: Biology; Genetics; Botany; Arabidopsis; Asexual reproduction; Genetic load; Inbreeding load; Microsatellite mutation rate; Mimulus

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

APA (6^th Edition):

Marriage, T. N. (2009). Mutation, asexual reproduction and genetic load: A study in three parts. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/5949

Chicago Manual of Style (16^th Edition):

Marriage, Tara N. “Mutation, asexual reproduction and genetic load: A study in three parts.” 2009. Doctoral Dissertation, University of Kansas. Accessed January 21, 2021. http://hdl.handle.net/1808/5949.

MLA Handbook (7^th Edition):

Marriage, Tara N. “Mutation, asexual reproduction and genetic load: A study in three parts.” 2009. Web. 21 Jan 2021.

Vancouver:

Marriage TN. Mutation, asexual reproduction and genetic load: A study in three parts. [Internet] [Doctoral dissertation]. University of Kansas; 2009. [cited 2021 Jan 21]. Available from: http://hdl.handle.net/1808/5949.

Council of Science Editors:

Marriage TN. Mutation, asexual reproduction and genetic load: A study in three parts. [Doctoral Dissertation]. University of Kansas; 2009. Available from: http://hdl.handle.net/1808/5949

University of Kansas

8. 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 (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 21, 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. 21 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 21]. 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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