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University of Arizona
1.
Vaishampayan, Prajakta.
Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/632210 
► Many nutrients including glucose, phosphate and amino acids regulate TORC1 activity and when the cells are in stress or starvation conditions, TORC1 activity is inhibited.…
(more)
▼ Many nutrients including glucose, phosphate and amino acids regulate TORC1 activity and
when the cells are in stress or starvation conditions, TORC1 activity is inhibited. It remains
unclear how this happens. So, we are interested in mapping the signaling system that talks
to TORC1 to ultimately understand how the complex integrates signals to control growth
in stress conditions. In this project, the response of TORC1 under nitrogen, glucose and
phosphate starvation conditions was checked in strains lacking one or more stress signaling
pathway proteins to identify the mechanism which leads to inhibition of TORC1 in stress
conditions.
Advisors/Committee Members: Capaldi, Andrew (advisor), Capaldi, Andrew (committeemember), Gutenkunst, Ryan (committeemember), Paek, Andrew (committeemember).
Subjects/Keywords: cell and molecular biology
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APA (6th Edition):
Vaishampayan, P. (2019). Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/632210
Chicago Manual of Style (16th Edition):
Vaishampayan, Prajakta. “Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
.” 2019. Masters Thesis, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/632210.
MLA Handbook (7th Edition):
Vaishampayan, Prajakta. “Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
.” 2019. Web. 19 Jan 2021.
Vancouver:
Vaishampayan P. Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
. [Internet] [Masters thesis]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/632210.
Council of Science Editors:
Vaishampayan P. Upstream Regulators of TORC1 Signaling Pathway in Saccharomyces cerevisiae
. [Masters Thesis]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/632210
University of Arizona
2.
Kunkel, Joseph.
A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
.
Degree: 2015, University of Arizona
URL: http://hdl.handle.net/10150/578637
► One of the leading aims of systems biology is the complete delineation of the organization and architecture of signaling networks. Within this aim, characterizing integrated…
(more)
▼ One of the leading aims of systems biology is the complete delineation of the organization and architecture of signaling networks. Within this aim, characterizing integrated circuits is a particular challenge. Integrated circuits are the sites of information multiplexing, where input from multiple sources are combined into a single output or channel. A number of quantitative methods for analyzing epistasis within integrated pathways have been developed, with limited success. Here I present Expression Component Analysis, a novel approach for determining quantitative epistasis within an integrated signaling circuit, and describe the application of Expression Component Analysis in analyzing an interesting and important integrated signaling circuit in the model eukaryote, S.cerevisiae.
Advisors/Committee Members: Capaldi, Andrew (advisor), Capaldi, Andrew (committeemember), Dieckmann, Carol (committeemember), Nagy, Lisa (committeemember), Weinert, Ted (committeemember).
Subjects/Keywords: circuit;
epistasis;
network;
Saccharomyces;
systems;
Genetics;
cerevisiae
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APA (6th Edition):
Kunkel, J. (2015). A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/578637
Chicago Manual of Style (16th Edition):
Kunkel, Joseph. “A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
.” 2015. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/578637.
MLA Handbook (7th Edition):
Kunkel, Joseph. “A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
.” 2015. Web. 19 Jan 2021.
Vancouver:
Kunkel J. A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
. [Internet] [Doctoral dissertation]. University of Arizona; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/578637.
Council of Science Editors:
Kunkel J. A Systems Approach for Dissecting Integrated Signaling Pathways: TORC1 and Ras/PKA Regulation of Glucose Induced Growth Control in S. cerevisiae
. [Doctoral Dissertation]. University of Arizona; 2015. Available from: http://hdl.handle.net/10150/578637
University of Arizona
3.
Monasky, Ross Calvin.
The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
.
Degree: 2018, University of Arizona
URL: http://hdl.handle.net/10150/628172
► Enteropathogenic Escherichia coli (EPEC) is a leading cause of infantile diarrhea, particularly in developing countries. EPEC belongs to the attaching and effacing (A/E) family of…
(more)
▼ Enteropathogenic Escherichia coli (EPEC) is a leading cause of infantile diarrhea, particularly in developing countries. EPEC belongs to the attaching and effacing (A/E) family of pathogens and harbors a type III secretion system (T3SS) that delivers virulence proteins directly into host epithelial cells. These proteins alter host structure and function, likely facilitating pathogenesis. We recently demonstrated that EspH, an EPEC secreted protein, is a critical virulence factor and that mutant strains lacking espH are impaired for pathogenesis. EspH induces host cell death through activation of caspases and mitochondrial fission. We hypothesizes that a wide range of host proteins are implicated in this cell death phenotype. Quantitation of host cell death during EPEC infection using siRNA-mediated knockdown of individual host cell proteins supports this hypothesis. A broad group of host protein knockdowns displayed altered host cell death during infection. The goal of my studies is to identify the host pathway(s) altered during EspH-induced epithelial cell death and, eventually, to establish the significance of this pathway in EPEC virulence.
Advisors/Committee Members: Viswanathan, V.K (advisor), Vedantam, Gayatri (committeemember), Capaldi, Andrew (committeemember).
Subjects/Keywords: Apoptosis;
EPEC;
siRNA
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APA (6th Edition):
Monasky, R. C. (2018). The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/628172
Chicago Manual of Style (16th Edition):
Monasky, Ross Calvin. “The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
.” 2018. Masters Thesis, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/628172.
MLA Handbook (7th Edition):
Monasky, Ross Calvin. “The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
.” 2018. Web. 19 Jan 2021.
Vancouver:
Monasky RC. The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
. [Internet] [Masters thesis]. University of Arizona; 2018. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/628172.
Council of Science Editors:
Monasky RC. The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence
. [Masters Thesis]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/628172
University of Arizona
4.
Woods, Dana.
Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/632540
► Cancer is quickly becoming the leading cause of death in the United States. Despite research making headway with early detection techniques and effective treatments, the…
(more)
▼ Cancer is quickly becoming the leading cause of death in the United States. Despite research making headway with early detection techniques and effective treatments, the number of cancer deaths per year continues to increase. There is still a lot we do not know about the mechanisms of cancer initiation and progression. A relatively recent field of study is epigenetics, or changes that occur outside of the DNA sequence. One such change is the expression or depletion of non-coding RNAs (ncRNAs). One type of ncRNA is long non-coding RNAs (lncRNAs), and several studies have linked lncRNA overexpression or downregulation to cancer progression. Mortal Obligate RNA Transcript, or MORT, is a lncRNA that has only recently been studied. Previous reports have shown lower levels of MORT in cancerous cell lines compared to normal cell lines, but very little additional information is known about the means by which it contributes to cancer progression. Our goal was to determine the localization and mechanism of MORT, specifically as it pertained to the mortal (non-tumorigenic) to immortal (tumorigenic) transition of human mammary epithelial cells. We observed that MORT loss occurs even earlier than previously thought, possibly priming the cells to bypass certain barriers necessary for tumorigenesis. MORT also seems to work in a complex with Poly(rC)-Binding Protein 1 (PCBP1) to somehow regulate certain mRNAs. Further, polysome profile analyses of MORT indicate that two populations of MORT exist within the cell; one with monosomes and one with polysomes. These results have important implications for detecting cancer as well as for understanding cancer progression mechanisms, possibly leading us to pursue therapeutic approaches involving MORT and its mechanisms of action.
Advisors/Committee Members: Futscher, Bernard (advisor), McEvoy, Justina (committeemember), Capaldi, Andrew (committeemember).
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APA ·
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Export
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Manager
APA (6th Edition):
Woods, D. (2019). Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/632540
Chicago Manual of Style (16th Edition):
Woods, Dana. “Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
.” 2019. Masters Thesis, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/632540.
MLA Handbook (7th Edition):
Woods, Dana. “Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
.” 2019. Web. 19 Jan 2021.
Vancouver:
Woods D. Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
. [Internet] [Masters thesis]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/632540.
Council of Science Editors:
Woods D. Localization and Mechanism of MORT in Human Mammary Epithelial Cell Mortal to Immortal Transition
. [Masters Thesis]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/632540
University of Arizona
5.
Diesing, Jessica Marie.
Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/632556
► Given the key role of integral membrane proteins as transporters, channels, and signal transducers, it is necessary to understand their function and characteristics. Interestingly, approximately…
(more)
▼ Given the key role of integral membrane proteins as transporters, channels, and signal transducers, it is necessary to understand their function and characteristics. Interestingly, approximately 30% of all proteins are membrane proteins, but there are very few fully characterized membrane proteins. This disparity is due to the practical problems of working with membrane proteins, specifically difficulties with expressing, solubilizing, and purifying. Thus, we have designed a simplified way to express membrane proteins using E coli. and purify them using ion exchange column chromatography followed by size exclusion chromatography. This purification technique results in concentrated fractions containing a maximum of four membrane proteins each which allows for easier analysis. The analysis of these endogenous proteins was performed using native top down mass spectrometry in hopes of identifying the proteins in the mixture and to identify their post translational modifications. I was able to find the mass of certain membrane proteins, but I was unable to analyze the MS2 spectra from these proteins. This is due to the fact that native top down mass spectrometry of larger membrane proteins can produce complex spectra that become difficult to analyze and match with a database given the current available software. This study gives an overview on the complexities of collecting and analyzing data from a mixture of unknown membrane proteins.
Advisors/Committee Members: Marty, Michael T (advisor), Dieckmann, Carol (committeemember), Capaldi, Andrew (committeemember).
Subjects/Keywords: Mass Spectrometry;
Top-down
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APA ·
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Export
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APA (6th Edition):
Diesing, J. M. (2019). Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/632556
Chicago Manual of Style (16th Edition):
Diesing, Jessica Marie. “Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
.” 2019. Masters Thesis, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/632556.
MLA Handbook (7th Edition):
Diesing, Jessica Marie. “Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
.” 2019. Web. 19 Jan 2021.
Vancouver:
Diesing JM. Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
. [Internet] [Masters thesis]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/632556.
Council of Science Editors:
Diesing JM. Using Top-Down Mass Spectrometry to Identify and Characterize Endogenous Membrane Protein Complexes
. [Masters Thesis]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/632556
University of Arizona
6.
Bellomo, Dante Anthony.
Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
.
Degree: 2020, University of Arizona
URL: http://hdl.handle.net/10150/642098
► FoxO1 is a signaling transcription factor regulated by the growth factor/PI3K/AKT pathway. Phosphorylation of FOXO1 by the serine/threonine kinase AKT, sequesters FOXO1 in the cytoplasm…
(more)
▼ FoxO1 is a signaling transcription factor regulated by the growth factor/PI3K/AKT pathway. Phosphorylation of FOXO1 by the serine/threonine kinase AKT, sequesters FOXO1 in the cytoplasm by blocking the interaction of FOXO1’s nuclear localization signal (NLS) with nuclear transport receptors and promoting FOXO1 binding to the cytoplasmic 14-3-3 proteins. Dephosphorylation of FOXO1 by the phosphatase PP2A restores NLS function and leads to accumulation of FOXO1 in the nucleus. Here, we use fluorescently labeled FOXO1 to characterize its nuclear trafficking dynamics under conditions of AKT and PP2A inhibition in order to describe the relative cytoplasmic dephosphorylation rate by PP2A and relative nuclear phosphorylation rate by AKT on FOXO1 respectively. Measured results affirm previous data that indicates AKT is less active in the nucleus than the cytoplasm and suggests that FOXO1 may undergo rapid shuttling into and out of the nucleus even during AKT activation.
Advisors/Committee Members: Paek, Andrew L (advisor), Weinert, Ted A. (committeemember), Capaldi, Andrew P. (committeemember).
Subjects/Keywords: AKT;
dynamics;
FOXO1;
nucleus;
protein;
trafficking
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APA ·
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APA (6th Edition):
Bellomo, D. A. (2020). Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/642098
Chicago Manual of Style (16th Edition):
Bellomo, Dante Anthony. “Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
.” 2020. Masters Thesis, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/642098.
MLA Handbook (7th Edition):
Bellomo, Dante Anthony. “Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
.” 2020. Web. 19 Jan 2021.
Vancouver:
Bellomo DA. Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
. [Internet] [Masters thesis]. University of Arizona; 2020. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/642098.
Council of Science Editors:
Bellomo DA. Estimating the Rate of FOXO1 Phosphorylation and Dephosphorylation Using Live Cell Imaging
. [Masters Thesis]. University of Arizona; 2020. Available from: http://hdl.handle.net/10150/642098
University of Arizona
7.
Thompson, Mark David.
Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
.
Degree: 2016, University of Arizona
URL: http://hdl.handle.net/10150/620817
► The eyespot of the single-celled alga Chlamydomonas aids the cell in detecting the direction of light in the environment. The complex assembly and asymmetric placement…
(more)
▼ The eyespot of the single-celled alga Chlamydomonas aids the cell in detecting the direction of light in the environment. The complex assembly and asymmetric placement of the eyespot provides a model to ask questions about assembly and asymmetric placement of organelles. Understanding the mechanisms that underlie assembly and asymmetric placement of the eyespot can be applied more broadly to their functions in other eukaryotic organisms. This study sought to understand the role of a key protein in those processes, Channelrhodopsin-1 (ChR1). ChR1 was found to localize along the entire length of the D4 rootlet from the region around the daughter basal body to the eyespot. ChR1 was found to primarily localize to the plasma membrane side of the D4, suggesting that ChR1 was being pulled through the plasma membrane from the region around the basal bodies to the eyespot. Further, ChR1 was found to be able to localize to the eyespot even with the truncation of the large cytoplasmic C-terminal domain, suggesting that ChR1 is able to complex with another protein that is being trafficked to the eyespot. One such protein was thought to be ChR2, the other light-activated ion channel localized to the eyespot. Efforts to isolate a mutation in ChR2 were unsuccessful. Initial efforts were made in this dissertation to perform proteomic studies of ChR1 and identify its interacting partners. ChR1 is not the master regulator of either placement or assembly of the eyespot, but work in this study lays the groundwork to further investigate transport of ChR1 and interacting proteins to the eyespot and their role in assembly of the eyespot.
Advisors/Committee Members: Dieckmann, Carol (advisor), Capaldi, Andrew (committeemember), Schroeder, Joyce (committeemember), Weinert, Ted (committeemember).
Subjects/Keywords: ChR1;
Eyespot;
Molecular & Cellular Biology;
Chlamydomonas
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APA ·
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APA (6th Edition):
Thompson, M. D. (2016). Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/620817
Chicago Manual of Style (16th Edition):
Thompson, Mark David. “Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
.” 2016. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/620817.
MLA Handbook (7th Edition):
Thompson, Mark David. “Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
.” 2016. Web. 19 Jan 2021.
Vancouver:
Thompson MD. Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
. [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/620817.
Council of Science Editors:
Thompson MD. Channelrhodopsin-1: Cellular Localization and Role in Eyespot Assembly and Placement in Chlamydomonas reinhardtii
. [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/620817
University of Arizona
8.
Langston, Rachel Elizabeth.
DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
.
Degree: 2016, University of Arizona
URL: http://hdl.handle.net/10150/622910
► Errors in DNA replication can cause chromosome instability and gross chromosomal rearrangements (GCRs). For my thesis work I investigate how chromosome instability can originate in…
(more)
▼ Errors in DNA replication can cause chromosome instability and gross chromosomal rearrangements (GCRs). For my thesis work I investigate how chromosome instability can originate in the telomere. Here I report how defects in Cdc13, a telomere specific protein, lead to chromosome instability and GCRs in Saccharomyces cerevisiae. Using a temperature sensitive mutant of Cdc13, I find that cdc13-induced instability can be induced in a single cell cycle and synergizes with replication stress (dNTP depletion via hydroxyurea). Additionally, I find that Cdc13 has to be functional during the cell’s S phase to suppress chromosome instability. Further genetic analysis suggests that that cdc13-induced chromosome instability depends on the generation of single stranded (ss)DNA, but not on the activity of canonical double strand break (DSB) repair pathways such as homologous recombination or non-homologous end joining. Finally, I demonstrate that telomeric unstable chromosomes can later progress and trigger rearrangements at centromeric loci. This system, using the conditional nature of the cdc13 mutation, promises a more complex analysis of the ontogeny of chromosome instability: in this case from errors semi-conservative DNA replication through the telomere to the formation and resolution of unstable chromosomes.
Advisors/Committee Members: Weinert, Ted (advisor), Weinert, Ted (committeemember), Capaldi, Andrew (committeemember), Bolger, Tim (committeemember), Beilstein, Mark (committeemember).
Subjects/Keywords: DNA replication;
telomere;
Chromosome instability
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APA (6th Edition):
Langston, R. E. (2016). DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/622910
Chicago Manual of Style (16th Edition):
Langston, Rachel Elizabeth. “DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
.” 2016. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/622910.
MLA Handbook (7th Edition):
Langston, Rachel Elizabeth. “DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
.” 2016. Web. 19 Jan 2021.
Vancouver:
Langston RE. DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
. [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/622910.
Council of Science Editors:
Langston RE. DNA Replication Defects in the Telomere Induce Chromosome Instability in a Single Cell Cycle
. [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/622910
University of Arizona
9.
Zeltzer, Sebastian Lauren.
HCMV Induced Alterations to Endocytic Sorting
.
Degree: 2018, University of Arizona
URL: http://hdl.handle.net/10150/627731
► The maintenance of cell surface proteins is critical to the ability of a cell to sense and respond to information in its environment. As such,…
(more)
▼ The maintenance of cell surface proteins is critical to the ability of a cell to sense and respond to information in its environment. As such, modulation of cell surface composition and receptor trafficking is a potentially important target of control in virus infection. Sorting endosomes (SEs) are control stations regulating the recycling or degradation of internalized plasma membrane proteins. Here we report that human cytomegalovirus (HCMV), a ubiquitous beta herpesvirus, alters the fate of internalized clathrin-independent endocytosis (CIE) cargo proteins, retaining them in virally reprogrammed SEs. We show that the small G protein ARF6, a regulator of CIE trafficking, is highly associated with SE membranes, relative to uninfected cells. This finding suggests that ARF6 and CIE cargo egress from the SE is diminished by infection. Over expression of the ubiquitin specific protease (USP) 6, also known as TRE17, was sufficient to restore ARF6 and some ARF6 cargo trafficking to the cell surface in infected cells. The USP-activity of TRE17 is required to rescue both ARF6 and associated cargo from SE retention in infection. Intriguingly, TRE17 expression does not affect all CIE cargos retained at SEs in infection. Although TRE17 mediates the trafficking of internalized major histocompatibility complex type I (MHCI) to the cell surface in uninfected cells, MHCI is insensitive to TRE17-mediated trafficking in the context of HCMV infection. These findings demonstrate a reprogramming of endocytic trafficking by HCMV infection and suggests that HCMV hijacks the normal sorting machinery and selectively sorts specific cargos into endocytic micro-domains that are subject to alternate sorting fates.
Advisors/Committee Members: Goodrum, Felicia D (advisor), Antin, Parker (committeemember), Capaldi, Andrew (committeemember), Koshy, Anita (committeemember), Wilson, Jean (committeemember).
Subjects/Keywords: ARF6;
CIE;
EEA1;
Endosome;
TRE17
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APA ·
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Zeltzer, S. L. (2018). HCMV Induced Alterations to Endocytic Sorting
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/627731
Chicago Manual of Style (16th Edition):
Zeltzer, Sebastian Lauren. “HCMV Induced Alterations to Endocytic Sorting
.” 2018. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/627731.
MLA Handbook (7th Edition):
Zeltzer, Sebastian Lauren. “HCMV Induced Alterations to Endocytic Sorting
.” 2018. Web. 19 Jan 2021.
Vancouver:
Zeltzer SL. HCMV Induced Alterations to Endocytic Sorting
. [Internet] [Doctoral dissertation]. University of Arizona; 2018. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/627731.
Council of Science Editors:
Zeltzer SL. HCMV Induced Alterations to Endocytic Sorting
. [Doctoral Dissertation]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/627731
University of Arizona
10.
Sullivan, Arron.
Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
.
Degree: 2018, University of Arizona
URL: http://hdl.handle.net/10150/631470
► The Target of Rapamycin Complex 1 (TORC1) is a master regulator of cellular growth in eukaryotes. Much insight has been gained into how amino acid…
(more)
▼ The Target of Rapamycin Complex 1 (TORC1) is a master regulator of cellular growth in eukaryotes. Much insight has been gained into how amino acid and nitrogen levels regulate TORC1 through the escape from rapamycin-induced growth arrest complex (EGOC), and its regulators including the Seh1-associated complex (SEAC). However, other nutrient levels and environmental stresses also act on TORC1, and far less is known about how these signals are transmitted to the complex. In two projects presented here we investigate the osmotic stress signaling network acting on TORC1 as well as regulators of TORC1 agglomeration that act in glucose and nitrogen starvation conditions.
In the first investigation, we introduce a novel and reproducible high-throughput assay to screen for genes that affect TORC1 activity in stress conditions. We then use these methods to measure the expression of a TORC1 dependent ribosome biogenesis gene, NSR1, in ~4700 strains from the yeast knock-out library during osmotic stress. We show that 440 of these strains are not able to properly repress NSR1 transcription. The genes identified in the screen form a highly-connected network including 17 proteins that directly interact with TORC1. Secondary rapamycin-based assays performed on these strains allowed us to further characterize the network and show that more than 50 of the proteins act downstream of TORC1. The data derived from this work serve as a resource for our lab and others studying TORC1, and the assay itself is customizable and can be used to characterize any gene regulatory network.
In the second study, we sought to further our understanding of the movement of TORC1 from its position distributed across the surface of the vacuolar membrane to a single agglomerate (TORC1-body) in starvation conditions. Previous work suggested that the AMPK in yeast, Snf1, indirectly promoted the phosphorylation of the TORC1 component Kog1. This phosphorylation event sped up aggregation of the complex by ~20 fold. In order to identify other signaling proteins that regulate TORC1-body formation we performed a screen examining the impact that nearly all non-essential kinases and phosphatases in yeast, as well as selected proteins from the previous high-throughput network, have on TORC1 agglomeration. We identified 13 new regulators of TORC1 body formation, including the PI(3)P binding protein Pib2. We also examined the impact of EGOC deletions and mutants had on body formation and discovered that active EGOC was an inhibitor of TORC1 aggregation. Together, we show that seven of the new regulators likely act at or above the EGOC dependent inhibition of TORC1 body formation; while others act at a later step to assist in body formation.
Advisors/Committee Members: Capaldi, Andrew P (advisor), Gutenkunst, Ryan (committeemember), Tax, Frans (committeemember), Weinert, Ted (committeemember), Yao, Guang (committeemember).
Subjects/Keywords: TORC1
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APA (6th Edition):
Sullivan, A. (2018). Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/631470
Chicago Manual of Style (16th Edition):
Sullivan, Arron. “Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
.” 2018. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/631470.
MLA Handbook (7th Edition):
Sullivan, Arron. “Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
.” 2018. Web. 19 Jan 2021.
Vancouver:
Sullivan A. Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
. [Internet] [Doctoral dissertation]. University of Arizona; 2018. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/631470.
Council of Science Editors:
Sullivan A. Multilayered Regulation of TORC1 Signaling in Saccharomyces cerevisiae
. [Doctoral Dissertation]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/631470
11.
Xiong, Kun.
Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/633130
► Non-adaptive evolution refers to evolutionary processes that are primarily driven not by natural selection, but by factors such as a bias towards generating certain mutations…
(more)
▼ Non-adaptive evolution refers to evolutionary processes that are primarily driven not by natural selection, but by factors such as a bias towards generating certain mutations over others. Although non-adaptive evolution is supported by abundant data, it is obscure outside the field of evolutionary biology, potentially for historical reasons. Considering non-adaptive evolution helps us to understand the origins and roles of traits at molecular and cellular levels, where research is often dominated by adaptationist assumptions. To demonstrate that a balanced view on evolution is necessary, my thesis research asks how adaptive and non-adaptive evolution shape the control of gene expression. I start by simulating the evolution of mechanisms for quality control of gene expression. I show that the error rate associated with gene expression is determined by both the mutational bias that tends to increase the error rate and by the effective population size of the species, which determines the strength of natural selection on the error rate. This offers an explanation for the observed non-monotonic relationship between transcriptional error rate and effective population size. I next study the evolution of transcriptional regulatory networks (TRNs). The adaptationist view hypothesizes that the enrichment of a subnetwork called coherent type 1 feed-forward loops (C1-FFLs) in TRNs is an adaptation for filtering out short spurious signals, but this and similar hypotheses about other enriched subnetworks are widely questioned by evolutionary biologists, because the adaptive hypothesis fails to consider network topologies that evolve non-adaptively. To help resolve this debate, I developed a highly mechanistic computational model that captures non-adaptive factors that can shape the topology of TRNs. I show that functional C1-FFLs evolve readily under selection for filtering out a spurious signal, but not under control selection conditions. While this result supports the adaptive origin of C1-FFLs, I show that non-adaptive subnetworks can also be enriched in TRNs evolved for filtering out a spurious signal, suggesting that inferring functions of TRNs from topology alone can be problematic. A further complication comes from the fact that a subnetwork that is topologically different from C1-FFLs also evolves to filter out spurious signals. In conclusion, I argue that non-adaptive evolution can explain the origins and roles of traits that are difficult to understand under adaptationism, and that considering non-adaptive evolution is necessary to carry out scientific research in all fields of biology. Molecular and cellular biologists should actively consider non-adaptive evolution in their research.
Advisors/Committee Members: Masel, Joanna (advisor), Gutenkunst, Ryan (committeemember), Yao, Guang (committeemember), Capaldi, Andrew (committeemember).
Subjects/Keywords: computational modeling;
drift barrier;
feed-forward loops;
Gene regulatory networks
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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APA (6th Edition):
Xiong, K. (2019). Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/633130
Chicago Manual of Style (16th Edition):
Xiong, Kun. “Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
.” 2019. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/633130.
MLA Handbook (7th Edition):
Xiong, Kun. “Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
.” 2019. Web. 19 Jan 2021.
Vancouver:
Xiong K. Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
. [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/633130.
Council of Science Editors:
Xiong K. Adaptive and Non-Adaptive Evolution of the Control of Gene Expression
. [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/633130
University of Arizona
12.
Eshleman, Nichole L.
Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/634222
► The regulation of mRNA levels is a key aspect of gene expression control and is determined by the processes of transcription and mRNA decay. Changes…
(more)
▼ The regulation of mRNA levels is a key aspect of gene expression control and is determined by the processes of transcription and mRNA decay. Changes in these two processes can cause widespread changes in gene expression. Nevertheless, how some mRNAs are specifically targeted for degradation, particularly under cellular stress, is still unclear. Furthermore, How nuclear mRNA processing events dictate cytoplasmic mRNA fate is also an area with many unanswered questions. Here I present several studies that specifically take a closer look at the various mechanisms behind degradation of mRNAs in the cytoplasm.
Chapter 2 describes how mutations in 3’ end processing and nuclear export factors (THO/TREX-2) causes aberrant mRNA-protein (mRNP) foci to form in the cytoplasm. These granules (termed TT foci) are composed of components found within stress granules (SGs) but are less dynamic in nature, as suggested by their resistance to cycloheximide-induced disassembly. TT foci are cleared by autophagy, suggesting a potentially novel mechanism of quality control to degrade aberrant mRNAs that escape nuclear degradation pathways and enter the cytoplasm.
Next, chapter 3 looks at how common mechanisms used for determining mRNA half-life cause changes in major signaling pathways, specifically looking at the TORC1, Hog1, and PKC pathways. Chemical inhibitors such as 1,10 phenanthroline and thiolutin show the strongest effects and inhibits TORC1 and PKC signaling but activates Hog1 signaling. 4-thiouracil (4tU), which is used to metabolically label mRNAs and assess mRNA decay or transcription rates, causes an increase in Processing bodies (PBs). Given that signaling pathways can regulate mRNA decay, our findings suggest more research is needed in yeast to determine an easy-to-use system to probe the contributions of various signaling pathways on mRNA decay without generating experimental artifacts.
Lastly, Chapter 4 is an ongoing study that examines at the role of TORC1 signaling in regulating decay of Ribosome Biogenesis (Ribi) mRNAs through the mRNA binding protein Puf4. However, due to our findings in Chapter 3, untangling the exact contribution of TORC1 on mRNA stability has been challenging. However, we present data indicating that both Puf4 and TORC1 can facilitate decay of the Ribi mRNA NSR1, and that Puf4 binding to NSR1’s 3’UTR is required for this regulation. However, Puf4 binding to NSR1 mRNA does not change in the presence or absence of TORC1 signaling. This suggests altered interactions of Puf4 with mRNA decay factors may be crucial and may be modified by TORC1 signaling, an area of immediate future interest.
Advisors/Committee Members: Buchan, Ross (advisor), Bolger, Tim (committeemember), Capaldi, Andrew (committeemember), Tax, Frans (committeemember), Beilstein, Mark (committeemember).
Subjects/Keywords: mRNA;
mRNA Decay;
Nuclear Quality Control;
Signaling
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Eshleman, N. L. (2019). Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/634222
Chicago Manual of Style (16th Edition):
Eshleman, Nichole L. “Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
.” 2019. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/634222.
MLA Handbook (7th Edition):
Eshleman, Nichole L. “Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
.” 2019. Web. 19 Jan 2021.
Vancouver:
Eshleman NL. Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
. [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/634222.
Council of Science Editors:
Eshleman NL. Ways to Kill the Messenger: Unraveling the Regulation of Cytoplasmic mRNA Decay
. [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/634222
University of Arizona
13.
Fernandes, Nikita Oswald.
mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
.
Degree: 2020, University of Arizona
URL: http://hdl.handle.net/10150/648638
► Post-transcriptional processes are crucial in the regulation of gene expression. Messenger ribonucleoprotein (mRNP) granules are dynamic, self-assembling membraneless organelles that harbor non-translating mRNAs implicated in…
(more)
▼ Post-transcriptional processes are crucial in the regulation of gene expression. Messenger ribonucleoprotein (mRNP) granules are dynamic, self-assembling membraneless organelles that harbor non-translating mRNAs implicated in multiple post-transcriptional processes like mRNA translation, repression, localization and turnover. Besides their involvement in cytoplasmic mRNA biology, mRNP granules are also associated with disease such as neurodegenerative diseases and cancer. In this thesis, we focus on P-bodies (PBs) and stress granules (SGs) studying their assembly, composition and relevance to disease.
In Chapter 2, we studied PB assembly and found that a specific mRNA RPS28B is important for P-body assembly by acting as a scaffold that enhances the interaction between Edc3, an important PB assembly protein recruited to the RPS28B 3’UTR, with Rps28 protein being translated off of the mRNA. The Edc3-Rps28 interaction correlates with PB assembly. Our work suggests that PBs may be preferentially nucleated by specific mRNA scaffolds, possibly a common theme in mRNP granule assembly. Furthermore, this is the first description, in yeast, of a cis-translated protein interacting with a protein recruited to the 3’UTR of the same mRNA, which in turn has functional consequences for assembly of cellular structures.
In Chapter 3, we studied the composition of SGs with the long term goal of uncovering additional functions of SGs. We developed novel SG purification protocols that are more accurate and sensitive in identifying SG components than previously published protocols. We have identified novel SG proteins that suggest that SGs could have roles in modulating translation during stress by altering the cellular tRNA charging status and cell cycle progression by sequestering Cdc28/CDK kinases, an area of immediate future interest.
In Chapter 4, we studied the relevance of SGs to neurodegenerative disease. We examined the claims that SGs are important for TDP-43 aggregation and toxicity associated with ALS. We looked at SG mutants and overexpression of SG proteins with regards to TDP-43 toxicity and aggregate formation in an established yeast model and in mammalian cell lines and found that SG assembly facilitates but is not required for TDP43 aggregation.
Advisors/Committee Members: Buchan, John Ross (advisor), Bolger, Timothy A. (committeemember), Capaldi, Andrew (committeemember), Khanna, May (committeemember), Zarnescu, Daniela C. (committeemember).
Subjects/Keywords: ALS;
mRNA scaffolds;
P-bodies;
Stress granules;
TDP-43
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Fernandes, N. O. (2020). mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/648638
Chicago Manual of Style (16th Edition):
Fernandes, Nikita Oswald. “mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
.” 2020. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/648638.
MLA Handbook (7th Edition):
Fernandes, Nikita Oswald. “mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
.” 2020. Web. 19 Jan 2021.
Vancouver:
Fernandes NO. mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
. [Internet] [Doctoral dissertation]. University of Arizona; 2020. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/648638.
Council of Science Editors:
Fernandes NO. mRNP Granules: Novel Insights Into Assembly, Composition and Relevance to Disease
. [Doctoral Dissertation]. University of Arizona; 2020. Available from: http://hdl.handle.net/10150/648638
University of Arizona
14.
Jain, Saumya.
The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
.
Degree: 2015, University of Arizona
URL: http://hdl.handle.net/10150/556224
► A recurring theme in biology is the aggregation of mRNA-protein complexes (mRNPs) into higher order assemblies. Often these complexes play important roles in the regulation…
(more)
▼ A recurring theme in biology is the aggregation of mRNA-protein complexes (mRNPs) into higher order assemblies. Often these complexes play important roles in the regulation of gene expression, but the function of the conserved cytoplasmic mRNP assemblies - P bodies and stress granules, is not known. It is believed that the misregulation of granule assembly is related to disorders like Amyotrophic Lateral Sclerosis and Frontotemporal Lobe Degeneration. Determining the complete composition of these granules may hold the key to understanding the function and mechanism of assembly of these granules. This work describes multiple approaches taken to identify new protein and mRNA components of P bodies and stress granules. New members of the P body and stress granule proteome reveal a role for these granules in diverse cellular processes including signal transduction, transcription and metabolism. Additionally, a new stress granule resident complex - the CCT complex, was also identified as a novel regulator of granule disassembly. This work also describes the first purification scheme for stress granules and presents a new system for in vitro study of stress granules. Together, the findings shed new light on the composition, function, structure and regulation of P bodies and stress granules in yeast.
Advisors/Committee Members: Fares, Hanna (advisor), Parker, Roy (advisor), Fares, Hanna (committeemember), Parker, Roy (committeemember), Weinert, Ted (committeemember), Capaldi, Andrew (committeemember), Zarnescu, Daniela (committeemember).
Subjects/Keywords: P Bodies;
Stress Granules;
Molecular & Cellular Biology;
mRNA binding proteins
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jain, S. (2015). The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/556224
Chicago Manual of Style (16th Edition):
Jain, Saumya. “The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
.” 2015. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/556224.
MLA Handbook (7th Edition):
Jain, Saumya. “The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
.” 2015. Web. 19 Jan 2021.
Vancouver:
Jain S. The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
. [Internet] [Doctoral dissertation]. University of Arizona; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/556224.
Council of Science Editors:
Jain S. The Analysis of mRNP Granule Composition and Structure in Saccharomyces cerevisiae
. [Doctoral Dissertation]. University of Arizona; 2015. Available from: http://hdl.handle.net/10150/556224
University of Arizona
15.
Norton, Jennifer Diane.
Mechanisms of Prion Variant Competition
.
Degree: 2017, University of Arizona
URL: http://hdl.handle.net/10150/625845
► The assembly of some misfolded proteins into aggregates can cause dramatic changes in cellular phenotypes. In prion diseases, these phenotypes are self-perpetuating because the highly…
(more)
▼ The assembly of some misfolded proteins into aggregates can cause dramatic changes in cellular phenotypes. In prion diseases, these phenotypes are self-perpetuating because the highly ordered aggregates are capable of templating the conversion of soluble form of the protein into the aggregated form. Interestingly, the aggregated form of the protein can exist as a range of unique self-replicating conformations, referred to as prion "strains" or "variants," conferring distinct phenotypic characteristics to their hosts. The presence of more than one prion variant has been implicated in the alteration of prion phenotypes, interspecies transmission and anti-prion drug-resistance. When more than one variant arises or is introduced into the same host, usually the faster replicating variant phenotypically dominates over slower replicating variants; however, this dominance is not absolute. Studies in mammals suggest that these outcomes are determined by competition between variants for the conversion of soluble protein. However, other steps in prion replication have not been thoroughly examined. In this study we show that prion variant dominance is indeed determined by competing for the conversion of soluble protein, but this advantage arises from other cell-based factors that influence prion biogenesis, such as fragmentation rates and the number of templates present within the cell.
Advisors/Committee Members: Serio, Tricia (advisor), Serio, Tricia (committeemember), Capaldi, Andrew (committeemember), Cordes, Matthew (committeemember), Krieg, Paul (committeemember), Weinert, Ted (committeemember).
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Norton, J. D. (2017). Mechanisms of Prion Variant Competition
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/625845
Chicago Manual of Style (16th Edition):
Norton, Jennifer Diane. “Mechanisms of Prion Variant Competition
.” 2017. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/625845.
MLA Handbook (7th Edition):
Norton, Jennifer Diane. “Mechanisms of Prion Variant Competition
.” 2017. Web. 19 Jan 2021.
Vancouver:
Norton JD. Mechanisms of Prion Variant Competition
. [Internet] [Doctoral dissertation]. University of Arizona; 2017. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/625845.
Council of Science Editors:
Norton JD. Mechanisms of Prion Variant Competition
. [Doctoral Dissertation]. University of Arizona; 2017. Available from: http://hdl.handle.net/10150/625845
University of Arizona
16.
Myers, Candace Tamara.
Origins and Development of the Embryonic Vascular System in Xenopus
.
Degree: 2013, University of Arizona
URL: http://hdl.handle.net/10150/299095
► Each step of vascular development needs to be carefully regulated; endothelial precursors must be specified, these cells then proliferate and coalesce to form vascular cords,…
(more)
▼ Each step of vascular development needs to be carefully regulated; endothelial precursors must be specified, these cells then proliferate and coalesce to form vascular cords, and finally they lumenate, undergo angiogenic branching and remodeling, and recruit smooth muscle cells to establish a mature vessel. An aberration at any of these steps during embryonic development is incompatible with life, and vascular pathologies in the adult are associated with numerous diseases including stroke, arteriosclerosis, diabetic retinopathies and cancer progression. My work has aimed to understand how endothelial precursors are specified, and more precisely the cell-signaling pathways and transcriptional networks that guide their fate. This work leads us to conclude the following: (1) blood island precursor cells in the Xenopus embryo can give rise to either blood or endothelial cells, and it is BMP-mediated activation of the erythroid transcriptional program that regulates cell fate, (2) endothelial specification requires the Ets transcription factor Etv2. Persistence of Etv2 expression in blood/endothelial cell precursors allows these cells to develop into endothelium, and overexpression of Etv2 in any of the three germ layers causes activation of every endothelial marker examined. Along the way we have characterized a number of small-molecule inhibitors that should be useful to the Xenopus community and applicable to other model systems.
Advisors/Committee Members: Krieg, Paul A (advisor), Antin, Parker (committeemember), Capaldi, Andrew (committeemember), Gregorio, Carol (committeemember), McDermott, Kim (committeemember), Tax, Frans (committeemember), Krieg, Paul A. (committeemember).
Subjects/Keywords: hemangioblast;
vasculogenesis;
Molecular & Cellular Biology;
endothelium
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Myers, C. T. (2013). Origins and Development of the Embryonic Vascular System in Xenopus
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/299095
Chicago Manual of Style (16th Edition):
Myers, Candace Tamara. “Origins and Development of the Embryonic Vascular System in Xenopus
.” 2013. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/299095.
MLA Handbook (7th Edition):
Myers, Candace Tamara. “Origins and Development of the Embryonic Vascular System in Xenopus
.” 2013. Web. 19 Jan 2021.
Vancouver:
Myers CT. Origins and Development of the Embryonic Vascular System in Xenopus
. [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/299095.
Council of Science Editors:
Myers CT. Origins and Development of the Embryonic Vascular System in Xenopus
. [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/299095
University of Arizona
17.
Ge, Xuezhen.
Chaperone Limitations in Prion Curing
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/636677
► Amyloid promotes a dramatic transition in protein conformation that perpetuates, giving rise to a broad variety of distinct phenotypes, ranging from pathological disorders to dynamic…
(more)
▼ Amyloid promotes a dramatic transition in protein conformation that perpetuates, giving rise to a broad variety of distinct phenotypes, ranging from pathological disorders to dynamic heritable traits. Amyloid has long been thought to be resistant to clearance by the proteostasis network, but increasing evidence is challenging this view. For example, heat shock disassembles yeast prion amyloids, revealing in vivo solubilization of these aggregates. However, the exact proteostatic niche that promotes amyloid clearance is largely unknown. We identified several environmental stresses leading to prion curing via the same mechanism as heat shock and further showed that a shared characteristic was the activation of the transcription factor heat shock factor 1 (Hsf1). Strikingly, artificial Hsf1 activation interfered with heat shock-mediated prion curing, presumably due to overexpression of a nucleotide exchange factor Sse1. Limiting Sse1, which decelerates the Hsp70 cycle, promoted chaperone loading on prion aggregates and enabled artificial Hsf1 activation to resolve prion aggregates; in contrast, it impaired resolution of stress-induced aggregates and cell growth at elevated temperature. Thus, our study demonstrates that the proteostasis network, fine-tuned for optimal dissolution of non-amyloid aggregates, can be reconfigured for solubilization of amyloid by modulating the Hsp70 cycle.
Advisors/Committee Members: Capaldi, Andrew P (advisor), Serio, Tricia R. (committeemember), Buchan, Ross J. (committeemember), Chapman, Eli (committeemember), Dieckmann, Carol L. (committeemember).
Record Details
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ge, X. (2019). Chaperone Limitations in Prion Curing
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/636677
Chicago Manual of Style (16th Edition):
Ge, Xuezhen. “Chaperone Limitations in Prion Curing
.” 2019. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/636677.
MLA Handbook (7th Edition):
Ge, Xuezhen. “Chaperone Limitations in Prion Curing
.” 2019. Web. 19 Jan 2021.
Vancouver:
Ge X. Chaperone Limitations in Prion Curing
. [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/636677.
Council of Science Editors:
Ge X. Chaperone Limitations in Prion Curing
. [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/636677
University of Arizona
18.
Pagliarulo, Christopher Lawrence.
TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
.
Degree: 2011, University of Arizona
URL: http://hdl.handle.net/10150/202773
► Traditional undergraduate biology courses are content intensive, requiring students to understand and remember large amounts of information in short periods of time. Yet most students…
(more)
▼ Traditional undergraduate biology courses are content intensive, requiring students to understand and remember large amounts of information in short periods of time. Yet most students maintain little of the material encountered during their education. Poor knowledge retention is a main cause of academic failure and high undergraduate attrition rates. Characterizing strategies that support robust learning is critical for ensuring student success. One such strategy is testing effect, the observation that repeated testing can improve the fidelity and durability of retained knowledge more than an equal quantity of restudy. Numerous investigations have described the nature and boundaries of testing effect. Very few, however, have characterized its efficacy in actual classroom practice. The current study investigated whether repeated testing or repeated study affected student retention and understanding of complex biological concepts. The study was conducted in a large (~320 students) introductory biology class. All study conditions and assessments were required components of the course. Student retention of two fundamental molecular biology "big ideas" was targeted; (1) the relationship between genotype and phenotype, and (2) the relationship between gene expression and cell function. Students were randomly assigned to one of three repeated quiz or study conditions. For four weeks, students encountered various combinations of multiple-choice (MC) questions and review material related to big ideas 1&2 and/or unrelated lecture topics. Five weeks after the last quiz, all students completed identical MC final exam questions related to both big ideas. To determine the quality of "understanding" assessed by the MC questions, a subset of students also completed a short answer (SA) test prior to the final exam. Both question formats assessed the same knowledge (2 big ideas) at the same level (comprehension and application). Final exam performance supported the finding that repeated retrieval improves long-term retention of knowledge relative to repeated study. Novel to other previous work conducted at the undergraduate level, the current findings suggest that repeated testing affects student retention and understanding of sophisticated concepts. Careful design and analysis of parallel multiple-choice and short answer questions demonstrated that each can target and elicit similar qualities and types of knowledge.
Advisors/Committee Members: Tomanek, Debra J (advisor), Elfring, Lisa K. (committeemember), Tax, Frans E. (committeemember), Capaldi, Andrew P. (committeemember), Pimentel, Angel C. (committeemember), Tomanek, Debra J. (committeemember).
Subjects/Keywords: multiple-choice;
Testing effect;
undergraduate;
Molecular & Cellular Biology;
complex ideas;
learning
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APA (6th Edition):
Pagliarulo, C. L. (2011). TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/202773
Chicago Manual of Style (16th Edition):
Pagliarulo, Christopher Lawrence. “TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
.” 2011. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/202773.
MLA Handbook (7th Edition):
Pagliarulo, Christopher Lawrence. “TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
.” 2011. Web. 19 Jan 2021.
Vancouver:
Pagliarulo CL. TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
. [Internet] [Doctoral dissertation]. University of Arizona; 2011. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/202773.
Council of Science Editors:
Pagliarulo CL. TESTING EFFECT AND COMPLEX COMPREHENSION IN A LARGE INTRODUCTORY UNDERGRADUATE BIOLOGY COURSE
. [Doctoral Dissertation]. University of Arizona; 2011. Available from: http://hdl.handle.net/10150/202773
19.
Hughes Hallett, James.
Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
.
Degree: 2015, University of Arizona
URL: http://hdl.handle.net/10150/556430
► The target of rapamycin complex I (TORC1) regulates cell growth and metabolism in all eukaryotes. Previous studies have shown that nitrogen and amino acid signals…
(more)
▼ The target of rapamycin complex I (TORC1) regulates cell growth and metabolism in all eukaryotes. Previous studies have shown that nitrogen and amino acid signals activate TORC1 via three GTPases; Gtr1, Gtr2, and Rho1, and the SEA-associated Npr2/3 proteins. However, little is known about the way that other nutrient or stress signals are transmitted to TORC1. Here I present two studies identifying how, and at what level, glucose and other environmental stimuli act to tune TORC1 signaling. In the first study I show that the TORC1 pathway populates three additional stress/starvation states. First, in glucose starvation conditions, the AMP-activated protein kinase (AMPK/Snf1) and at least one other factor push the TORC1 pathway into an off state, in which Sch9-branch signaling and PP2A-branch signaling are both inhibited. The TORC1 pathway remains in the glucose starvation state even when cells are simultaneously starved for nitrogen and glucose or treated with rapamycin. Second, in osmotic stress, the MAPK Hog1/p38 drives the TORC1 pathway into a different state, in which Sch9 signaling and PP2A-branch signaling are inhibited, but PP2A-branch signaling can still be activated by nitrogen starvation. Third, in oxidative stress and heat stress, TORC1-Sch9 signaling is blocked while weak PP2A-branch signaling occurs. Together, the data show that the TORC1 pathway acts as an information-processing hub, activating different genes in different conditions to ensure that available energy is allocated to drive growth, amino acid synthesis, or a stress response, depending on the needs of the cell. In the second study I investigate further the observed hierarchy of TORC1 inputs. I show that glucose starvation triggers disassembly of TORC1, and movement of the key TORC1 component Kog1, to a single body near the edge of the vacuole. These events are driven by AMPK/Snf1-dependent phosphorylation of Kog1 at Serine 491/494 and two nearby prion-like motifs. Kog1-bodies then serve to increase the threshold for TORC1 activation in cells that have been starved for a significant period of time. Together, this data shows that Kog1-bodies create hysteresis (memory) in the TORC1 pathway and help ensure that cells remain committed to a quiescent state under suboptimal conditions.
Advisors/Committee Members: Capaldi, Andrew (advisor), Capaldi, Andrew (committeemember), Montfort, William (committeemember), Nagy, Lisa (committeemember), Serio, Tricia (committeemember), Weinert, Ted (committeemember).
Subjects/Keywords: Molecular & Cellular Biology
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hughes Hallett, J. (2015). Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/556430
Chicago Manual of Style (16th Edition):
Hughes Hallett, James. “Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
.” 2015. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/556430.
MLA Handbook (7th Edition):
Hughes Hallett, James. “Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
.” 2015. Web. 19 Jan 2021.
Vancouver:
Hughes Hallett J. Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
. [Internet] [Doctoral dissertation]. University of Arizona; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/556430.
Council of Science Editors:
Hughes Hallett J. Systems Level Analysis of TORC1 Pathway Signaling in S. cerevisiae
. [Doctoral Dissertation]. University of Arizona; 2015. Available from: http://hdl.handle.net/10150/556430
20.
Worley, Jeremy.
Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
.
Degree: 2015, University of Arizona
URL: http://hdl.handle.net/10150/577327
► To thrive when conditions are favorable and survive when they are stressful, cells must carefully regulate their growth rate and stress response programs. This requires…
(more)
▼ To thrive when conditions are favorable and survive when they are stressful, cells must carefully regulate their growth rate and stress response programs. This requires rapid, coordinated regulation of many genes in response to information about the levels of numerous nutrients and stress conditions. We are beginning to understand how, in eukaryotes, the TORC1 and PKA pathways regulate growth in nutrient rich conditions. However, how cells tune growth and stress responses in suboptimal conditions is largely unknown. To address this, we ran screens to begin reconstructing the growth regulation network in stress conditions. We found many novel regulators, including signaling proteins, components of the vacuolar ATPase, transcription factors, and components of the endomembrane system. In order to place these regulators in the TORC1 pathway, we performed follow up experiments on over 300 of these regulators using the TORC1 inhibitor rapamycin. We were able to place many new components in the TORC1 pathway, including 59 genes that act downstream of TORC1. We were particularly interested in the discovery that Vip1, a conserved inositol pyrophosphate kinase, was necessary for the shutdown of hundreds of growth genes in stress and starvation conditions. In subsequent experiments, we learned that the inositol pyrophosphate second messengers (including 1-PP-IP5, 5-PP-IP4, and 5-PP-IP5) are critical regulators of cell growth and the general stress response, acting in parallel to the TORC1 pathway to control the activity of the class I HDAC Rpd3L. Taken together, this work reveals many new regulators of cell growth and shows how delineation of one such regulator uncovered a global role for a little known family of second messengers.
Advisors/Committee Members: Capaldi, Andrew P (advisor), Capaldi, Andrew P. (committeemember), Dieckmann, Carol (committeemember), Tax, Frans (committeemember), Weinert, Ted (committeemember).
Subjects/Keywords: Molecular & Cellular Biology
…Molecular and Cellular Biology and the Functional Genomics Core facility, University of
Arizona…
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APA ·
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MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Worley, J. (2015). Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/577327
Chicago Manual of Style (16th Edition):
Worley, Jeremy. “Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
.” 2015. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/577327.
MLA Handbook (7th Edition):
Worley, Jeremy. “Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
.” 2015. Web. 19 Jan 2021.
Vancouver:
Worley J. Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
. [Internet] [Doctoral dissertation]. University of Arizona; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/577327.
Council of Science Editors:
Worley J. Reconstructing The S. Cerevisiae Growth Control Network In Stress Conditions
. [Doctoral Dissertation]. University of Arizona; 2015. Available from: http://hdl.handle.net/10150/577327
21.
Aryanpur, Peyman Paul.
Regulation of Ded1 Activity in Translation Initiation
.
Degree: 2019, University of Arizona
URL: http://hdl.handle.net/10150/631881
► DEAD-box RNA helicases are critical regulators of gene expression. The S. cerevisiae DEAD-box helicase Ded1 has long been used as a model to study the…
(more)
▼ DEAD-box RNA helicases are critical regulators of gene expression. The S. cerevisiae DEAD-box helicase Ded1 has long been used as a model to study the biochemical and biological functions of these enzymes. Here I present two paradigms of regulation for Ded1 activity: by the protein interaction with Gle1, and by the TORC1 signaling pathway.
In the first study I help elucidate the mechanism of Gle1 regulation of Ded1 in translation initiation. We show that GLE1 expression suppresses the repressive effects of DED1 in vivo and Gle1 counteracts Ded1 in translation assays in vitro. Furthermore, both Ded1 and Gle1 affect the assembly of preinitiation complexes. Through mutation analysis and binding assays, we show that Gle1 inhibits Ded1 by reducing its affinity for RNA. Our results are consistent with a model wherein active Ded1 promotes translation but inactive or excess Ded1 leads to translation repression.
In the second study I examine the role of Ded1 in the translational response to TORC1 inhibition and identify a novel function of Ded1 as a translation repressor. I show that C-terminal mutants of DED1 are defective in downregulating translation following TORC1 inhibition with rapamycin. Furthermore, following TORC1 inhibition, eIF4G1 normally dissociates from translation complexes and is degraded, and this process is attenuated in mutant cells. Mapping the functional requirements for Ded1 in this translational response indicates that Ded1 enzymatic activity and interaction with eIF4G1 are required, while homo-oligomerization may be dispensable. Our results are consistent with a model wherein, Ded1 stalls translation and specifically removes eIF4G1 from translation pre-initiation complexes, thus removing eIF4G1 from the translating mRNA pool and leading to the co-degradation of both proteins. Shared features among DED1 orthologs suggest that this role is conserved and may be implicated in pathologies such as oncogenesis.
Advisors/Committee Members: Bolger, Timothy A (advisor), Tax, Frans (committeemember), Capaldi, Andrew (committeemember), Montfort, Bill (committeemember), Zarnescu, Daniela (committeemember).
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Aryanpur, P. P. (2019). Regulation of Ded1 Activity in Translation Initiation
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/631881
Chicago Manual of Style (16th Edition):
Aryanpur, Peyman Paul. “Regulation of Ded1 Activity in Translation Initiation
.” 2019. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/631881.
MLA Handbook (7th Edition):
Aryanpur, Peyman Paul. “Regulation of Ded1 Activity in Translation Initiation
.” 2019. Web. 19 Jan 2021.
Vancouver:
Aryanpur PP. Regulation of Ded1 Activity in Translation Initiation
. [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/631881.
Council of Science Editors:
Aryanpur PP. Regulation of Ded1 Activity in Translation Initiation
. [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/631881
University of Arizona
22.
Bauer, Christopher Randal.
REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
.
Degree: 2009, University of Arizona
URL: http://hdl.handle.net/10150/194098
► Within the span of a single human lifetime, we have discovered that DNA is the basis of genetic inheritance, deciphered the genetic code, and determined…
(more)
▼ Within the span of a single human lifetime, we have discovered that DNA is the basis of genetic inheritance, deciphered the genetic code, and determined the entire sequence of multiple human genomes. However, we still have only a basic understanding of many of the processes that regulate DNA structure, function, and dynamics. The work presented in this dissertation describes the roles of two sets of genes that regulate the expression of genetic information and its transmission from one generation to the next.The condensin II complex has been implicated in the maintenance of genomic integrity during cell division and in transcriptional regulation during interphase. These roles stem from its ability to regulate chromosome structure though the mechanisms of this regulation are unclear. Evidence suggests that it is important for chromosome condensation and segregation during mitosis and meiosis. We have shown that this complex regulates the condensation of chromosomes during interphase. Its ability to reduce chromosome axial length provides a mechanism for the establishment of chromosome territories. We have also shown that condensin II differentially regulates interactions between homologous and heterologous DNA sequences. These findings contribute to our understanding of the overall structure of the nucleus, the regulation of chromosome structure, and the regulation of gene expression.The function of the Drosophila gene, sticky, is poorly understood. It contributes to cytokinesis by phosphorylating myosin II, but it also has a role in the regulation of chromatin structure. Mutations in sticky are associated with a wide range of developmental abnormalities. We provide evidence that this gene regulates the expression of numerous other genes which contribute to the phenotypes observed when sticky is mutated. We also show that sticky function overlaps with that of dfmr1, an ortholog of the gene associated with the most common form of human mental retardation. These findings contribute to our understanding of transcriptional regulation in chromatin and its implications in development and disease.
Advisors/Committee Members: Bosco, Giovanni (advisor), Parker, Roy (committeemember), Weinert, Ted (committeemember), Zarnescu, Daniela (committeemember), Capaldi, Andrew (committeemember).
Subjects/Keywords: chromatin;
condensin;
fmr;
nucleus;
sti
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bauer, C. R. (2009). REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194098
Chicago Manual of Style (16th Edition):
Bauer, Christopher Randal. “REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
.” 2009. Doctoral Dissertation, University of Arizona. Accessed January 19, 2021.
http://hdl.handle.net/10150/194098.
MLA Handbook (7th Edition):
Bauer, Christopher Randal. “REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
.” 2009. Web. 19 Jan 2021.
Vancouver:
Bauer CR. REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
. [Internet] [Doctoral dissertation]. University of Arizona; 2009. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10150/194098.
Council of Science Editors:
Bauer CR. REGULATION OF GENOMIC STRUCTURE AND TRANSCRIPTION IN DROSOPHILA
. [Doctoral Dissertation]. University of Arizona; 2009. Available from: http://hdl.handle.net/10150/194098
. 
Open Access Theses and Dissertations
