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University of California, Berkeley
1.
Thompson Exner, Cameron Ruth.
Coordination of patterning and morphogenesis during early development in Xenopus laevis.
Degree: 2017, University of California, Berkeley
URL: http://pqdtopen.proquest.com/#viewpdf?dispub=10192543 
► Over the course of development, cells and tissues of the embryo must take on the correct fates and morphologies to produce a functioning organism.…
(more)
▼ Over the course of development, cells and tissues of the embryo must take on the correct fates and morphologies to produce a functioning organism. The patterning events and morphogenetic processes that accomplish this task have been the subject of decades of research, the consequence of which has been a detailed comprehension of the molecular mechanisms that regulate each. Equally important is an understanding of the mechanisms that coordinate patterning with morphogenesis, such that they occur with the correct relative spatiotemporal dynamics. My thesis work sought to characterize such co-regulation in the context of two developmental events in a vertebrate model, the African clawed frog <i>Xenopus laevis:</i> induction of bottle cell formation at the onset of gastrulation after germ layer induction, and regulation of the morphogenetic movements of neurulation in relation to neural plate patterning. Chapter 1 of this dissertation provides a general introduction to the patterning and morphogenetic events of early development relevant to my thesis. Chapter 2 presents a discussion of my work to characterize the function of two signaling pathways, namely Nodal signaling and Wnt/Planar Cell Polarity, in the induction of bottle cells. My experiments confirm the requirement for Nodal signaling in bottle cell induction, but do not support a role for the individual transcriptional targets of Nodal signaling tested here or for Wnt/PCP. Chapter 3 summarizes my work to address the function of two transcription factor-encoding genes, <i>sall1</i> and <i> sall4,</i> in neural development, including their roles in anteroposterior neural patterning, neural tube morphogenesis, and neural differentiation. My work shows that both <i>sall1</i> and <i>sall4</i> are required for all three processes, and supports the hypothesis that their key role in this context is to transcriptionally repress stem cell factors of the <i>pou5f3</i> family, allowing progression through neural development. As a whole, this work summarizes my research to characterize molecules that co-regulate early patterning and morphogenetic events in the <i> X. laevis</i> embryo.
Subjects/Keywords: Molecular biology; Cellular biology; Developmental biology
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APA (6th Edition):
Thompson Exner, C. R. (2017). Coordination of patterning and morphogenesis during early development in Xenopus laevis. (Thesis). University of California, Berkeley. Retrieved from http://pqdtopen.proquest.com/#viewpdf?dispub=10192543
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Thompson Exner, Cameron Ruth. “Coordination of patterning and morphogenesis during early development in Xenopus laevis.” 2017. Thesis, University of California, Berkeley. Accessed January 19, 2020.
http://pqdtopen.proquest.com/#viewpdf?dispub=10192543.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Thompson Exner, Cameron Ruth. “Coordination of patterning and morphogenesis during early development in Xenopus laevis.” 2017. Web. 19 Jan 2020.
Vancouver:
Thompson Exner CR. Coordination of patterning and morphogenesis during early development in Xenopus laevis. [Internet] [Thesis]. University of California, Berkeley; 2017. [cited 2020 Jan 19].
Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10192543.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Thompson Exner CR. Coordination of patterning and morphogenesis during early development in Xenopus laevis. [Thesis]. University of California, Berkeley; 2017. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10192543
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Iowa State University
2.
Haage, Amanda Michelle.
Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells.
Degree: 2014, Iowa State University
URL: https://lib.dr.iastate.edu/etd/14152
► Currently there are no reliable treatment options for cancer metastasis. The complex cascade of events leading to metastasis reveals a multitude of therapeutic targets, but…
(more)
▼ Currently there are no reliable treatment options for cancer metastasis. The complex cascade of events leading to metastasis reveals a multitude of therapeutic targets, but few of these targets are extensively involved in as many steps as the matrix metalloproteinases (MMPs). The MMP family is the major extracellular matrix (ECM) remodeling enzymes utilized by normal and cancerous cell alike. A therapeutic technique aimed at MMPs has been the subject of much research, but remains elusive due to two major concerns: 1) MMPs are post-translationally activated, usually by other MMPs, resulting in convoluted catalytic networks where activity does not equate expression, and 2) lack of knowledge of both the specific and redundant roles of MMPs in particular microenvironments. Here I address both these concerns by using specific MMP activity probes and inhibitors to study how MMP activity is regulated by a variety of microenvironmental conditions including modulating both the ECM and the signaling factors available to the cells. With this study I have been able to demonstrate novel regulation of MMP activity by ECM stiffness and cellular contractility in pancreatic cancer cells. This response is mediated through a specific MMP, membrane-tethered one MMP (MT1-MMP), which activates secreted MMPs in response to mechanical stimulation. Finally I have shown that MMP activities are differentially modulated by growth factor stimulation and that whole cell MMP activity does not always correlate with localized ECM degradation. These findings bring cancer metastasis research another step closer to being able to effectively target MMPs for therapy.
Subjects/Keywords: Molecular, Cellular, and Developmental Biology; Cell Biology
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APA (6th Edition):
Haage, A. M. (2014). Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/14152
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Haage, Amanda Michelle. “Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells.” 2014. Thesis, Iowa State University. Accessed January 19, 2020.
https://lib.dr.iastate.edu/etd/14152.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Haage, Amanda Michelle. “Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells.” 2014. Web. 19 Jan 2020.
Vancouver:
Haage AM. Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells. [Internet] [Thesis]. Iowa State University; 2014. [cited 2020 Jan 19].
Available from: https://lib.dr.iastate.edu/etd/14152.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Haage AM. Microenvironment regulation of matrix metalloproteinase activity in pancreatic cancer cells. [Thesis]. Iowa State University; 2014. Available from: https://lib.dr.iastate.edu/etd/14152
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
3.
Do, Sylvia Vu.
Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico.
Degree: 2015, Iowa State University
URL: https://lib.dr.iastate.edu/etd/14337
► Evolution by natural selection and the overuse of antibiotics have led to the emergence and proliferation of drug-resistant bacteria. One of the mechanisms that bacteria…
(more)
▼ Evolution by natural selection and the overuse of antibiotics have led to the emergence and proliferation of drug-resistant bacteria. One of the mechanisms that bacteria have evolved to overcome antibiotics is the membrane efflux pump. By expelling the drugs outside of the cell, the bacterium prevents the molecule from accumulating to a toxic level. Transcriptional regulators, which control when the genes of these proteins are transcribed from DNA to RNA, are able to sense the drugs within the cell by binding to them. In the transcriptional repression process, once ligand-bound, the regulators are released from the DNA, allowing the efflux protein to be expressed. The efflux pump then recognizes these drugs and pumps them out of the cell. Both the regulator and the protein that it regulates recognize the same drugs. In fact, most of these are able to recognize multiple drugs or drug classes, making treatment difficult.
In this thesis, we examine the protein structure to determine its function and to predict its reaction to new substrates. We determined the X-ray crystal structures of the transcriptional regulator Rv3066 from Mycobacterium tuberculosis and two components of the MtrCDE tripartite pump (MtrD and MtrE) from Neisseria gonorrhoeae, and examined the tripartite efflux complex CusCBA to determine the mechanism behind ion extrusion. To better understand how the regulators and efflux pumps recognize their substrates, we used AutoDock Vina to predict binding sites and to predict possible new ligands. With this data, we hope to find a way to impede the resistance of bacteria to drugs and allow existing antibiotics to become effective again.
Subjects/Keywords: Molecular, Cellular, and Developmental Biology; Bioinformatics; Biology
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APA (6th Edition):
Do, S. V. (2015). Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/14337
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Do, Sylvia Vu. “Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico.” 2015. Thesis, Iowa State University. Accessed January 19, 2020.
https://lib.dr.iastate.edu/etd/14337.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Do, Sylvia Vu. “Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico.” 2015. Web. 19 Jan 2020.
Vancouver:
Do SV. Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico. [Internet] [Thesis]. Iowa State University; 2015. [cited 2020 Jan 19].
Available from: https://lib.dr.iastate.edu/etd/14337.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Do SV. Structural mechanisms of bacterial multidrug efflux pumps, their regulation, and implications for future research in silico. [Thesis]. Iowa State University; 2015. Available from: https://lib.dr.iastate.edu/etd/14337
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Washington
4.
Barsh, Gabrielle Russo.
Spatial and temporal mechanisms of vagus motor neuron topographic map development.
Degree: PhD, 2017, University of Washington
URL: http://hdl.handle.net/1773/40653
► Many networks throughout the nervous system are organized into topographic maps, where the positions of neuron cell bodies in the projecting field correspond with the…
(more)
▼ Many networks throughout the nervous system are organized into topographic maps, where the positions of neuron cell bodies in the projecting field correspond with the positions of their axons in the target field. Previous studies of topographic map development show evidence for spatial patterning mechanisms, in which gene expression patterns in the projecting and target fields determine axon targeting in a manner that depends on the precise positions of the cell bodies. Here, we describe a novel mechanism of topographic map formation that depends on the timing of axon outgrowth, and that is overlaid on spatial patterning mechanisms. We focus on the vagus motor neurons, which are topographically arranged in both mammals and fish. We show that cell position along the anterior-posterior axis of hindbrain rhombomere 8 determines expression of hox5 genes, which are expressed in posterior vagus motor neurons. Using live-imaging techniques in zebrafish embryos, we additionally reveal a difference in time of axon formation between anterior versus posterior motor neurons that is independent of neuron birth time. We show that hox5 expression directs topographic mapping without affecting time of axon outgrowth, and that time of axon outgrowth directs topographic mapping without affecting hox5 expression. The vagus motor neuron topographic map is therefore determined by two mechanisms that are acting in parallel: a hox5-dependent spatial mechanism akin to classic mechanisms of topographic map formation, and a novel axon outgrowth-dependent temporal mechanism in which time of axon formation is differentially regulated to direct axon targeting.
Advisors/Committee Members: Moens, Cecilia B (advisor).
Subjects/Keywords:
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APA (6th Edition):
Barsh, G. R. (2017). Spatial and temporal mechanisms of vagus motor neuron topographic map development. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/40653
Chicago Manual of Style (16th Edition):
Barsh, Gabrielle Russo. “Spatial and temporal mechanisms of vagus motor neuron topographic map development.” 2017. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/40653.
MLA Handbook (7th Edition):
Barsh, Gabrielle Russo. “Spatial and temporal mechanisms of vagus motor neuron topographic map development.” 2017. Web. 19 Jan 2020.
Vancouver:
Barsh GR. Spatial and temporal mechanisms of vagus motor neuron topographic map development. [Internet] [Doctoral dissertation]. University of Washington; 2017. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/40653.
Council of Science Editors:
Barsh GR. Spatial and temporal mechanisms of vagus motor neuron topographic map development. [Doctoral Dissertation]. University of Washington; 2017. Available from: http://hdl.handle.net/1773/40653
University of Minnesota
5.
Hsu, Wei-Shan.
Chromosome cohesion and condensation in Saccharomyces cerevisiae.
Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2011, University of Minnesota
URL: http://purl.umn.edu/115898
► Sister chromatid cohesion and chromosome condensation are two essential cell cycle processes for maintaining genome stability. Pds1 is the only known regulator for maintaining cohesion…
(more)
▼ Sister chromatid cohesion and chromosome condensation are two essential cell cycle processes for maintaining genome stability. Pds1 is the only known regulator for maintaining cohesion between sister chromatids during S phase till anaphase onset by inhibiting Esp1 activity, which is important for preventing aberrant chromosome segregation. However, pds1 null yeast are viable and able to keep cohesion during S phase. This indicates a redundant pathway maintains sister chromatid cohesion in the absence of Pds1. We have identified the Pds1-independent mechanism involved in S phase sister chromatid cohesion. This mechanism requires the function of two B-type cyclins, Clb5 and Clb6, as well as Cdc28. When DNA replication is efficient, either the Pds1- or Clb5/Clb6-dependent mechanism is sufficient to maintain sister chromatid cohesion. However, both mechanisms are required for S phase cohesion under conditions of replication stress. Further investigation revealed that cells lacking Clb5 and Clb6 have reduced levels of chromatin associated cohesin under conditions of replication stress. Further, this cohesion defect requires spindle tension to be observed by examining TRP1 locus separation. In conclusion, yeast cells maintain sister chromatid cohesion by a Clb5/Clb6 dependent mechanism for efficiently loading cohesin onto chromatin during S phase as well as a Pds1 dependent mechanism for inhibiting the protease activity of Esp1 before anaphase onset.
Chromosome condensation requires the function of the condesin complex. Recent studies mainly focused on the ATPase activity of condensin in introducing DNA supercoiling. We studied how condensin is regulated through the cell cycle. We found that the protein levels of condensin subunits are cell cycle regulated. Chromosomes condense in response to higher condensin protein abundance. Chromosome decondensation at the end of the cell cycle requires Smc4 proteolysis mediated by APC/C ubiquitin ligase. This Smc4 protein turnover needs the function of Mad2 in the absence of nocodazole, but Mad2 is dispensable for Smc4 proteolysis under conditions of pre-anaphase arrest in the presence of nocodazole. In addition to protein abundance, phospho modification of Smc4 by Cdc28 also regulates the timing of chromosome condensation. This phospho modification of Smc4 destabilized Smc4 protein as well as preventing premature chromosome condensation early in the cell cycle.
Collectively, we studied the underlying mechanisms of two essential events for genome stability: sister chromatid cohesion and chromosome condensation. Both events are under regulation by multiple mechanisms to ensure the faithfulness. Understanding these mechanisms using budding yeast would avail against the human diseases caused by genome instability.
Subjects/Keywords: Molecular; Cellular; Developmental Biology and Genetics
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APA ·
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Manager
APA (6th Edition):
Hsu, W. (2011). Chromosome cohesion and condensation in Saccharomyces cerevisiae. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/115898
Chicago Manual of Style (16th Edition):
Hsu, Wei-Shan. “Chromosome cohesion and condensation in Saccharomyces cerevisiae.” 2011. Doctoral Dissertation, University of Minnesota. Accessed January 19, 2020.
http://purl.umn.edu/115898.
MLA Handbook (7th Edition):
Hsu, Wei-Shan. “Chromosome cohesion and condensation in Saccharomyces cerevisiae.” 2011. Web. 19 Jan 2020.
Vancouver:
Hsu W. Chromosome cohesion and condensation in Saccharomyces cerevisiae. [Internet] [Doctoral dissertation]. University of Minnesota; 2011. [cited 2020 Jan 19].
Available from: http://purl.umn.edu/115898.
Council of Science Editors:
Hsu W. Chromosome cohesion and condensation in Saccharomyces cerevisiae. [Doctoral Dissertation]. University of Minnesota; 2011. Available from: http://purl.umn.edu/115898
University of Minnesota
6.
Buckley, Shannon Mychel.
Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells.
Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2009, University of Minnesota
URL: http://purl.umn.edu/99706
► The hematopoietic stem cell (HSC) maintains hematopoiesis throughout life. HSC are used to treat a number of hematopoietic disorders including leukemia and other hematopoietic malignancies,…
(more)
▼ The hematopoietic stem cell (HSC) maintains hematopoiesis throughout life. HSC are used to treat a number of hematopoietic disorders including leukemia and other hematopoietic malignancies, as well as immunodeficiencies. The first successful bone marrow (BM) transplantation was performed over 30 years ago. Even so, we still have an incomplete understanding of what regulates different aspects of HSC behavior. To repopulate the hematopoietic system, physicians initially used bone marrow (BM) as a cell source, and more recently granulocyte colony stimulating factor (G-CSF) mobilized peripheral blood (PB) cells, and umbilical cord blood (UCB). Although HSC transplantation can cure a significant proportion of patients, limitations still remain. Histocompatibility complex leukocyte antigen (HLA) matching is imperative to reduce the risk of graft versus host disease, such that a suitable donor cannot be found for many patients. Near complete matching is required when adult sources of cells are used, whereas, some degree of HLA-mismatch is allowed when UCB grafts are used, even though a low incidence of severe graft versus host disease (GVHD) persists following UCB transplantation. One of the problems related to the use of UCB as cell source is the limited number of HSC per graft, such that one UCB unit is insufficient to treat adult patients.
Therefore, many investigators have examined whether HSC can be expanded ex vivo, as this would circumvent the problem associated with the limited number of HSC present in UCB. However, robust methods for ex vivo maintenance, let alone HSC expansion, have not been developed. Understanding the mechanisms that regulate proliferation, self-renewal, and differentiation of HSC may yield means of HSC expansion in vitro, as well as, allow for a single cord blood graft to be used for an adult recipient, and aid in attempts for genetic modification of autologous HSC for therapy of genetic hematopoietic disorders. Theoretically, the potential to expand HSC in vitro could provide a limitless supply of HSC for therapy.
In vivo, HSC receive signals from the local microenvironment in which they reside that regulate self-renewal vs. differentiation. In adults, HSC reside in the BM, in putative stem cell niches. The hypothesis of the HSC niche was first proposed in 1978 by Schofield, who proposed that cell contact is required between HSC and cells in the niche for HSC maintenance. Over the last 5 years, two different locations have been identified within the adult BM that may serve as the BM niche: the endosteal niche and the vascular niche. Even less is known regarding putative stem cell niches during development. During development hematopoiesis is initiated in the yolk sac and the aorta-gonad-mesenephros (AGM) region. Around embryonic day (E) 12 in mouse, HSC migrate to the fetal liver (FL) where extensive expansion of the HSC pool occurs and HSC differentiate to the lineage committed progenitors. HSC migrate from the liver to the BM just before birth. As each of these microenvironments…
Subjects/Keywords: Molecular; Cellular; Developmental Biology and Genetics
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APA ·
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APA (6th Edition):
Buckley, S. M. (2009). Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/99706
Chicago Manual of Style (16th Edition):
Buckley, Shannon Mychel. “Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells.” 2009. Doctoral Dissertation, University of Minnesota. Accessed January 19, 2020.
http://purl.umn.edu/99706.
MLA Handbook (7th Edition):
Buckley, Shannon Mychel. “Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells.” 2009. Web. 19 Jan 2020.
Vancouver:
Buckley SM. Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells. [Internet] [Doctoral dissertation]. University of Minnesota; 2009. [cited 2020 Jan 19].
Available from: http://purl.umn.edu/99706.
Council of Science Editors:
Buckley SM. Identification of microenvironment factors that regulate hematopoietic stem and progenitor cells. [Doctoral Dissertation]. University of Minnesota; 2009. Available from: http://purl.umn.edu/99706
Virginia Commonwealth University
7.
Godfrey, Grayland W, II.
Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance.
Degree: MS, Biology, 2017, Virginia Commonwealth University
URL: https://scholarscompass.vcu.edu/etd/4841
► An essential process to the development of the neural network of the nervous system is axon guidance. The noncanonical Wnt/Planar Cell Polarity pathway has…
(more)
▼ An essential process to the development of the neural network of the nervous system is axon guidance. The noncanonical Wnt/Planar Cell Polarity pathway has been identified as an integral component in controlling the projection of axons during axon guidance. Prickle, ROR1 and ROR2 are PCP related proteins that do not have clearly defined roles in the process. This study aims to use zebrafish CoPA neurons as a model to study the roles of Prickle, ROR1, and ROR2 in axon guidance. Using in situ hybridization, morpholino knockdown, and CRISPR/Cas9 loss of function experiments were able to identify
ror1,
ror2 and
prickle as potential required components in CoPA neuron axon guidance. Elucidating the role of these protein in axon guidance not only will increase our knowledge of the PCP pathway but it will also increase our understanding of the development of the nervous system.
Advisors/Committee Members: Dr. Gregory Walsh, Dr. Jennifer Stewart, Dr. James Lister, Dr. Sarah Rothschild.
Subjects/Keywords: Biology; Developmental Neuroscience; Molecular and Cellular Neuroscience
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APA ·
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APA (6th Edition):
Godfrey, Grayland W, I. (2017). Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance. (Thesis). Virginia Commonwealth University. Retrieved from https://scholarscompass.vcu.edu/etd/4841
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Godfrey, Grayland W, II. “Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance.” 2017. Thesis, Virginia Commonwealth University. Accessed January 19, 2020.
https://scholarscompass.vcu.edu/etd/4841.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Godfrey, Grayland W, II. “Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance.” 2017. Web. 19 Jan 2020.
Vancouver:
Godfrey, Grayland W I. Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance. [Internet] [Thesis]. Virginia Commonwealth University; 2017. [cited 2020 Jan 19].
Available from: https://scholarscompass.vcu.edu/etd/4841.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Godfrey, Grayland W I. Characterizing the Role of Key Planar Cell Polarity Pathway Components in Axon Guidance. [Thesis]. Virginia Commonwealth University; 2017. Available from: https://scholarscompass.vcu.edu/etd/4841
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Michigan
8.
Yao, Zhiyuan.
Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae.
Degree: PhD, Molecular, Cellular, and Developmental Biology, 2018, University of Michigan
URL: http://hdl.handle.net/2027.42/144163
► Macroautophagy (hereafter autophagy), literally defined as a type of self-eating, is a dynamic cellular process in which cytoplasm is sequestered within a unique compartment termed…
(more)
▼ Macroautophagy (hereafter autophagy), literally defined as a type of self-eating, is a dynamic
cellular process in which cytoplasm is sequestered within a unique compartment termed the phagophore. Upon completion, the phagophore matures into a double-membrane autophagosome that fuses with the lysosome or vacuole, allowing degradation of the cargo. Autophagy is involved in various aspects of cell physiology, and its dysregulation is associated with a range of diseases. Thus, Understanding of
molecular mechanism and the regulation of autophagy is important for exploring potential therapy of diseases.
The most prominent feature of autophagy is the formation of a double-membrane sequestering compartment, the phagophore; this transient organelle surrounds part of the cytoplasm and matures into an autophagosome, which subsequently fuses with the vacuole or lysosome to allow degradation of the cargo. Much attention has focused on the process involved in phagophore nucleation and expansion, but many questions remain. Here, we identified the yeast protein Icy2, which we now name Atg41, as playing a role in autophagosome formation. Atg41 interacts with the transmembrane protein Atg9, a key component involved in autophagosome biogenesis, and both proteins display a similar localization profile. Under autophagy-inducing conditions the expression level of Atg41 increases dramatically and is regulated by the transcription factor Gcn4. This work provides further insight into the mechanism of Atg9 function and the dynamics of sequestering membrane formation during autophagy.
Autophagy is a tightly controlled
cellular process by which cytosolic proteins, Studies have revealed the
molecular mechanism of transcriptional regulation of autophagy-related (ATG) genes upon nutrient deprivation. However, little is known about their translational regulation. Here we found that Dhh1, a DExD/H-box RNA helicase, is required for efficient translation of Atg1 and Atg13, two proteins essential for autophagy induction. Dhh1 directly associates with ATG1 and ATG13 mRNAs under nitrogen starvation conditions. The structured regions shortly after the start codons of the two mRNAs are necessary for their regulation by Dhh1. Moreover, Eap1, an EIF4E binding protein, physically interacts with Dhh1 to facilitate the delivery of the Dhh1-ATG mRNA complex to the translation initiation machinery. These results suggest a model for how some ATG genes bypass the general translational suppression that occurs during nitrogen starvation to maintain a proper level of autophagy.
The
molecular mechansim of autophagosome formation has been an interesting topic over years due to its importance to autophagy process. This thesis enlarges the knowledge of Atg9 cycling system in yeast, which provides insight for understanding membrane donation process in autophagy. Diffterent levels of autophagy control are essential for
cellular homestasis. This thesis, by investigating both transcriptional and translational regulation of autophagy, provides insight in understanding…
Advisors/Committee Members: Klionsky, Daniel J (committee member), Weisman, Lois S (committee member), Olsen, Laura J (committee member), Xu, Haoxing (committee member).
Subjects/Keywords: Autophagy; Molecular, Cellular and Developmental Biology; Science
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APA ·
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MLA ·
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Yao, Z. (2018). Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/144163
Chicago Manual of Style (16th Edition):
Yao, Zhiyuan. “Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae.” 2018. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/144163.
MLA Handbook (7th Edition):
Yao, Zhiyuan. “Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae.” 2018. Web. 19 Jan 2020.
Vancouver:
Yao Z. Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae. [Internet] [Doctoral dissertation]. University of Michigan; 2018. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/144163.
Council of Science Editors:
Yao Z. Molecular Mechanism and Regulation of Autophagy in Saccharomyces cerevisiae. [Doctoral Dissertation]. University of Michigan; 2018. Available from: http://hdl.handle.net/2027.42/144163
Iowa State University
9.
Saldanha, Jenifer N.
Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans.
Degree: 2015, Iowa State University
URL: https://lib.dr.iastate.edu/etd/14488
► Organisms often encounter various forms of stress during their lifespan. The response to stress involves the regulation of cellular processes by stress response modulators that…
(more)
▼ Organisms often encounter various forms of stress during their lifespan. The response to stress involves the regulation of cellular processes by stress response modulators that function to ultimately enable resistance and survival. In this dissertation I used Caenorhabditis elegans as a model to study the effects of a variety of stresses including the response to cyanide, hypoxia, and hypergravity.
Chapter 2 of this thesis focuses on understanding the mechanisms of cyanide resistance in C. elegans. We employed a novel microfluidic device to describe the resistance phenotypes with greater spatio-temporal resolution. The results shed light on the underlying genetic bases that contribute to cyanide resistance, including the role of the hypoxia-inducible factor HIF-1. They also reveal new findings about the cyanide resistance phenotype, and help establish the applicability of microfluidic devices in studying the effects of aqueous toxicants in real-time.
Chapter 3 is a study investigating the crosstalk between the stress response modulators HIF-1, DAF-16, and HLH29 in C. elegans. We found significant over-representation of DAF-16 target genes, as well as HLH29 target genes in our lists of genes up- or down- regulated by hypoxia or in animals with over-active HIF-1. Genes identified in this study are known to play important roles in the response and resistance to diverse forms of stress. The findings from this study illustrate the complex mechanisms employed by cells to regulate the expression of subsets of genes in the response to specific forms of stress.
In chapter 4 we studied the effects of hypergravity exposure on C. elegans mobility, behavior, reproduction, and lifespan. We found that the animals rapidly recoverered mobility after short, intense bouts of hypergravity exposure, but their reproductive capabilities and lifespans were altered after longer durations of treatment. The results suggest that long term exposure to stress in the form of hypergravity may be detrimental to the animal's health and physiology.
Collectively, the results from my thesis help elucidate the important roles played by stress response mediators in contributing to an organism's survival. They also illustrate the rich and complex ways in which organisms modulate their responses to various forms of stress.
Subjects/Keywords: Molecular, Cellular, and Developmental Biology; Genetics
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APA (6th Edition):
Saldanha, J. N. (2015). Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/14488
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Saldanha, Jenifer N. “Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans.” 2015. Thesis, Iowa State University. Accessed January 19, 2020.
https://lib.dr.iastate.edu/etd/14488.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Saldanha, Jenifer N. “Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans.” 2015. Web. 19 Jan 2020.
Vancouver:
Saldanha JN. Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans. [Internet] [Thesis]. Iowa State University; 2015. [cited 2020 Jan 19].
Available from: https://lib.dr.iastate.edu/etd/14488.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Saldanha JN. Analyses of diverse stresses, including hypoxia, cyanide, and hypergravity in Caenorhabditis elegans. [Thesis]. Iowa State University; 2015. Available from: https://lib.dr.iastate.edu/etd/14488
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Washington
10.
Dennis, Shannon Marie.
C. elegans Germline Defense Against Retrotransposons.
Degree: PhD, 2012, University of Washington
URL: http://hdl.handle.net/1773/20776
► Nematodes appear to have efficient defenses against the germline activity of retroviruses and retrotransposons, as evidenced by the small number of sequences in their genome…
(more)
▼ Nematodes appear to have efficient defenses against the germline activity of retroviruses and retrotransposons, as evidenced by the small number of sequences in their genome derived from such elements. No viruses that infect the C. elegans germline have been discovered, nor has the presence of virus-like particles (VLPs) been previously reported in germ cells. Retroelements that infect non-dividing cells must access the nucleus via nuclear pores, and in nematode germ cells the majority of nuclear pores are clustered under ribonucleoprotein particles called P granules. In order to determine how retroelements confront or circumvent P granules, we first searched for strains with germline VLPs. We surveyed 16 wild strains of C. elegans and 4 additional Caenorhabditis species using electron microscopy. We discovered VLPs in the germlines of C. japonica and a few C. elegans strains, including the lab wild-type strain N2. Using RNA interference to knock-down candidate retrotransposons, we determined that the C. elegans VLPs are the product of Cer1, a Ty3/Gypsy class LTR retrotransposon. Expression of Cer1 is both temperature- and age-dependent. In conditions where Cer1 is abundantly expressed it contributes to programmed cell deaths that occur normally during germline development. The distribution of germline VLPs differed between C. japonica and C. elegans, suggesting different strategies for accumulation near the nucleus, were they might encounter free nuclear pores. In C. japonica, we found VLPs in clusters near P granules, indicating they may aggregate near P granules to gain nuclear proximity. In C. elegans, in contrast, the VLPs only accumulated near the nuclear envelope (NE) in post-pachytene germ cells, where P granule-free nuclear pores are being added to the NE. Additionally, C. elegans VLPs show a strong association with microtubules (MTs), and wild-type localization of VLPs is dynein-dependent. We propose that the C. elegans VLPs bind to MTs in order to resist cytoplasmic flow and probe for free nuclear pores. The studies described here provide a foundation for using the model C. elegans to study host-pathogen interactions between retroelements and germ cells.
Advisors/Committee Members: Priess, James R (advisor).
Subjects/Keywords: Molecular biology; Developmental biology; Virology; Molecular and cellular biology
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APA (6th Edition):
Dennis, S. M. (2012). C. elegans Germline Defense Against Retrotransposons. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/20776
Chicago Manual of Style (16th Edition):
Dennis, Shannon Marie. “C. elegans Germline Defense Against Retrotransposons.” 2012. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/20776.
MLA Handbook (7th Edition):
Dennis, Shannon Marie. “C. elegans Germline Defense Against Retrotransposons.” 2012. Web. 19 Jan 2020.
Vancouver:
Dennis SM. C. elegans Germline Defense Against Retrotransposons. [Internet] [Doctoral dissertation]. University of Washington; 2012. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/20776.
Council of Science Editors:
Dennis SM. C. elegans Germline Defense Against Retrotransposons. [Doctoral Dissertation]. University of Washington; 2012. Available from: http://hdl.handle.net/1773/20776
UCLA
11.
McDonald, Austin Ian.
Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta.
Degree: Molecular Biology, 2017, UCLA
URL: http://www.escholarship.org/uc/item/8n49s3ds
► Endothelial cells form a monolayer of cells on the luminal surface of blood vessels. Over the last several decades, investigators have reported numerous successes elucidating…
(more)
▼ Endothelial cells form a monolayer of cells on the luminal surface of blood vessels. Over the last several decades, investigators have reported numerous successes elucidating the cellular and molecular mechanisms by which endothelial cells can direct the sprouting formation of small capillary blood vessels (angiogenesis) with concomitant expansion of the total surface and number of cells composing the endothelial lining, with important implications for human disease. However the mechanisms which apply in the case of lining expansion in large arteries, the primary location for human atherosclerotic disease, is unknown. Knowledge of how the lining grows and regenerates damage under physiological conditions provides important insight into the failure of the lining in the diseased state. Progress in study of this process has been limited due to technical difficulties and challenges. Isolated endothelial cells grown in a dish have poor fidelity to the same cells in their native context of a pulsating artery. They lack circulating blood and the complex interactions between endothelial cells, vascular smooth muscle cells, and circulating blood cells. Meanwhile, the arteries of mammals, the gold standard for extrapolating to humans, are difficult to study due to the need for surgical access and a much more limited suite of experimental tools.This thesis addresses important unknowns in the biology of the mammalian endothelial lining of arteries using an in vivo mouse model. Specifically, it answers the following questions currently outstanding in the field of vascular biology: 1) When more endothelial cells come to exist in the endothelial lining, where do they originate? 2) Is there an endothelial stem or progenitor cell which persists past the embryonic stage to supply new endothelial cells to growing or damaged vessels? And 3) Does the expansion of the endothelial lining to cover new area within large vessels share the same molecular organization as angiogenesis?In Chapter 2, I present work which uses clonal cell tracing experiments to show that during the postnatal enlargement of the aorta, the largest vessel in the body, the division of existing endothelial cells within the arterial lining itself is sufficient to explain the entirety of the increase in length and circumference of the lining. In Chapter 4, I use a surgical method to damage the lining of the adult aorta and observe its regeneration. Through lineage tracing, parabiosis, and clonal tracing experiments I show that in fact a progenitor subpopulation exists within the adult arterial lining, and these cells supply the majority of the new endothelial lining. In Chapter 3, I report the results of molecular profiling of endothelial cells participating in the regeneration of the endothelial lining of the mouse aorta by transcriptomic sequencing, and follow up with immunocytochemistry validating the selective expression of key regulatory proteins in the regenerating lining and not in the surrounding lining or in the angiogenic neonatal mouse retina.In sum, my work…
Subjects/Keywords: Molecular biology; Cellular biology; Developmental biology; aorta; artery; cellular; endothelial; molecular; regeneration
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APA (6th Edition):
McDonald, A. I. (2017). Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/8n49s3ds
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
McDonald, Austin Ian. “Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta.” 2017. Thesis, UCLA. Accessed January 19, 2020.
http://www.escholarship.org/uc/item/8n49s3ds.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
McDonald, Austin Ian. “Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta.” 2017. Web. 19 Jan 2020.
Vancouver:
McDonald AI. Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta. [Internet] [Thesis]. UCLA; 2017. [cited 2020 Jan 19].
Available from: http://www.escholarship.org/uc/item/8n49s3ds.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
McDonald AI. Cellular and Molecular Basis for Postnatal Growth and Adult Regeneration of the Mouse Aorta. [Thesis]. UCLA; 2017. Available from: http://www.escholarship.org/uc/item/8n49s3ds
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Minnesota
12.
Joshi, Preeti Madhav.
Histone methylation in polycomb gene silencing.
Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2010, University of Minnesota
URL: http://purl.umn.edu/96716
► Polycomb (PcG) group proteins are chromatin-modifying factors that collaborate to repress gene expression during development. PcG proteins are crucial for silencing during animal embryogenesis, maintenance…
(more)
▼ Polycomb (PcG) group proteins are chromatin-modifying factors that collaborate to repress gene expression during development. PcG proteins are crucial for silencing during animal embryogenesis, maintenance of stem cell populations and are also implicated in cancer epigenetics.
PcG proteins operate in at least three molecular complexes: PHORC, PRC2 and PRC1. Current models suggest that PRC1 is recruited at target loci by PRC2 and is most directly responsible for gene silencing. Our study uses the Drosophila model system to investigate the precise role of PRC2 in PRC1 targeting.
One key function of PRC2 is to catalyze methylation of histone H3 on lysine-27. A common model suggests that this creates a binding site for the recruitment of PRC1. The loss of PRC2 leads to disruption in PcG mediated silencing. We wished to assess if PRC1 is recruited at PcG targets by a direct interaction with PRC2 or by binding to the methyl mark. We have used enzyme-dead versions of PRC2 that can stably accumulate at target loci and shown that PRC1 is also found at these targets suggesting that the initial recruitment of PRC1 is independent of PRC2 catalytic function. We have also engineered a heterologous enzyme, called vSET, to create methylated histones in the absence of PRC2. This heterologous enzyme can be used to test for PRC1 accumulation without PRC2.
Subjects/Keywords: Biochemistry; Chromatin Biology; Molecular Genetics; Molecular, Cellular, Developmental Biology and Genetics
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APA (6th Edition):
Joshi, P. M. (2010). Histone methylation in polycomb gene silencing. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/96716
Chicago Manual of Style (16th Edition):
Joshi, Preeti Madhav. “Histone methylation in polycomb gene silencing.” 2010. Doctoral Dissertation, University of Minnesota. Accessed January 19, 2020.
http://purl.umn.edu/96716.
MLA Handbook (7th Edition):
Joshi, Preeti Madhav. “Histone methylation in polycomb gene silencing.” 2010. Web. 19 Jan 2020.
Vancouver:
Joshi PM. Histone methylation in polycomb gene silencing. [Internet] [Doctoral dissertation]. University of Minnesota; 2010. [cited 2020 Jan 19].
Available from: http://purl.umn.edu/96716.
Council of Science Editors:
Joshi PM. Histone methylation in polycomb gene silencing. [Doctoral Dissertation]. University of Minnesota; 2010. Available from: http://purl.umn.edu/96716
13.
Gilmore, Richard F, III.
Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion.
Degree: MS, Molecular & Cellular Biology, 2011, University of Massachusetts
URL: https://scholarworks.umass.edu/theses/679
► The sexually dimorphic nucleus of the preoptic area (SDN-POA) was first discovered in rats and is one of the most famous and best studied…
(more)
▼ The sexually dimorphic nucleus of the preoptic area (SDN-POA) was first discovered in rats and is one of the most famous and best studied sex differences in the field of neuroscience. Though well documented in rats (larger in males than females), this sex difference was only recently able to be observed in mice due to the discovery of the protein calbindin-D28k as a marker. Recent studies have shown a larger, more distinct calbindin-immunoreactive (ir) cell cluster in male mice compared to females. However, the exact location of the cluster and whether the sex difference is one of total cell number or cell distribution remains unclear. In this study, we use defined contours to demonstrate that male mice have more calbindin-ir cells than females both in the central cell cluster and areas surrounding the cluster. We also report a full masculinization of these characteristics in females given a single injection of estradiol benzoate (EB) on the day of birth. The potential role of cell death in the development of this sex difference was tested using mice with a deletion of the
bax gene
, which codes for a pro death factor required for the establishment of other sex differences in the mouse brain. We demonstrate that
bax knockout (KO) mice have more cells in the POA region in general, but eliminating cell death does not affect the development of the sex difference in calbindin-ir cell number, nor does it affect calbindin-ir cell spread. Taken together, this suggests that cell death is not a significant underlying mechanism in the establishment of the sex difference in the calbindin-ir cell cluster in the mouse POA.
Advisors/Committee Members: Nancy G Forger, Geert J. DeVries.
Subjects/Keywords: Biochemistry; Cell Biology; Developmental Neuroscience; Molecular and Cellular Neuroscience; Molecular Biology
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APA (6th Edition):
Gilmore, Richard F, I. (2011). Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion. (Masters Thesis). University of Massachusetts. Retrieved from https://scholarworks.umass.edu/theses/679
Chicago Manual of Style (16th Edition):
Gilmore, Richard F, III. “Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion.” 2011. Masters Thesis, University of Massachusetts. Accessed January 19, 2020.
https://scholarworks.umass.edu/theses/679.
MLA Handbook (7th Edition):
Gilmore, Richard F, III. “Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion.” 2011. Web. 19 Jan 2020.
Vancouver:
Gilmore, Richard F I. Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion. [Internet] [Masters thesis]. University of Massachusetts; 2011. [cited 2020 Jan 19].
Available from: https://scholarworks.umass.edu/theses/679.
Council of Science Editors:
Gilmore, Richard F I. Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion. [Masters Thesis]. University of Massachusetts; 2011. Available from: https://scholarworks.umass.edu/theses/679
University of Michigan
14.
Sant, Karilyn E.
Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment.
Degree: PhD, Toxicology, 2014, University of Michigan
URL: http://hdl.handle.net/2027.42/110498
► Mono-2-ethylhexyl phthalate (MEHP) is the primary metabolite of di-2-ethylhexyl phthalate (DEHP), a ubiquitous toxicant used in the production of plastics. Studies have associated prenatal phthalate…
(more)
▼ Mono-2-ethylhexyl phthalate (MEHP) is the primary metabolite of di-2-ethylhexyl phthalate (DEHP), a ubiquitous toxicant used in the production of plastics. Studies have associated prenatal phthalate exposure with a spectrum of adverse health outcomes including neurodevelopmental disorders, although mechanisms are unknown. The importance of adequate fetal nutrition for neurodevelopment has been well-studied, but the role of histiotrophic nutrition pathways (HNPs) in embryonic development is not well characterized. This work aimed to 1) characterize mechanisms by which nutrient starvation may alter epigenetic programming during development, 2) evaluate the teratogenic potential of MEHP exposure, 3) examine MEHP’s impact on HNPs and epigenetic programming, and 4) contrast the transcriptomic and epigenomic effects of MEHP exposure and adverse neurodevelopmental outcomes. Whole embryo culture was used to investigate rodent conceptuses during early organogenesis. Treatment with leupeptin, a protease inhibitor known to decrease HNPs, altered one-carbon (C1) metabolism and decreased global DNA methylation in the embryo (EMB) and visceral yolk sac (VYS). MEHP treatment reduced embryonic growth, increased the prevalence of open neural tubes (NTD) in EMB, and increased susceptibility to oxidation. After 6-h MEHP treatment, decreased EMB and VYS expression of genes in pathways involved in the metabolism of amino acids, energy metabolism, and oxidative phosphorylation occurred. Total HNP function, defined as the clearance of extra-conceptal proteins into the conceptal tissues and fluids, was reduced in a dose-dependent manner after 3-h MEHP treatment. C1 metabolism was increased by 24-h MEHP treatment, suggesting time-dependent response in nutrient uptake and metabolism due to exposures. Global embryonic DNA methylation was decreased after 24 h exposure to MEHP and in EMB with NTDs. Global histone methylation at the H3K4 and H3K27 loci was increased in EMBs with NTDs and treated VYSs. Parallel transcriptomic and epigenomic analysis examined the effects of MEHP treatment and also NTD status. Pathway analysis of expression and DNA methylation data revealed disrupted nutrient metabolism, increased xenobiotic metabolism, and induction of pathways governing
cellular fate such as increased autophagy. This research demonstrates that MEHP may induce nutrient starvation and redox control of autophagy (NSRCA), and these findings suggest that NSRCA may play a crucial role in teratogenesis.
Advisors/Committee Members: Harris, Craig (committee member), Dolinoy, Dana (committee member), Sartor, Maureen A. (committee member), Caruso, Rita Loch (committee member).
Subjects/Keywords: Developmental toxicology; Embryonic nutrition; Molecular, Cellular and Developmental Biology; Health Sciences
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APA (6th Edition):
Sant, K. E. (2014). Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/110498
Chicago Manual of Style (16th Edition):
Sant, Karilyn E. “Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment.” 2014. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/110498.
MLA Handbook (7th Edition):
Sant, Karilyn E. “Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment.” 2014. Web. 19 Jan 2020.
Vancouver:
Sant KE. Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment. [Internet] [Doctoral dissertation]. University of Michigan; 2014. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/110498.
Council of Science Editors:
Sant KE. Acute Embryotoxicity of Mono-2-Ethylhexyl Phthalate (MEHP) in Mice: Nutrition, Epigenomics, and Environment. [Doctoral Dissertation]. University of Michigan; 2014. Available from: http://hdl.handle.net/2027.42/110498
University of Michigan
15.
Macara, Ann Marie.
Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits.
Degree: PhD, Molecular, Cellular and Developmental Biology, 2016, University of Michigan
URL: http://hdl.handle.net/2027.42/133489
► I aim to understand the interaction between the environment and the developing brain through investigating how sensory experience shapes behavior. Sensory experience modifies neural connections…
(more)
▼ I aim to understand the interaction between the environment and the developing brain through investigating how sensory experience shapes behavior. Sensory experience modifies neural connections through activity-dependent plasticity, enabling animals to cope with environmental variability. Classic work, particularly those in vertebrate visual systems, has provided important insights into the mechanisms that underlie experience-dependent plasticity of the developing circuit. However, there are significant gaps explaining the mechanism by which sensory experience shapes circuit function during development. This dissertation examines how sensory experience during development changes the sensorimotor circuit to shape behavior in Drosophila melanogaster. Drosophila provides a relatively simple and genetically amenable model for analyzing both neural development and mechanisms underlying behaviors, and is thus a powerful model for discovering basic principles underlying experience-dependent plasticity during development. To address how sensory stimuli alters the sensorimotor circuit, I have established a calcium live-imaging technique to physiologically measure neural dynamics within larval brains and have developed a behavioral assay to probe motor output. Through the use of these experimental techniques, I have determined that sensory experience during a sensitive period in development modifies behavior through an intrinsic program of circuit development. These findings suggest that the development of the larval sensorimotor circuit is shaped by sensory input and neural activity.
Advisors/Committee Members: Cadigan, Kenneth M (committee member), Ye, Bing (committee member), Moenter, Sue (committee member), Kuwada, John Y (committee member), Collins, Catherine A (committee member).
Subjects/Keywords: Drosophila melanogaster; developmental neurobiology; Molecular, Cellular and Developmental Biology; Science
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APA ·
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APA (6th Edition):
Macara, A. M. (2016). Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/133489
Chicago Manual of Style (16th Edition):
Macara, Ann Marie. “Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits.” 2016. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/133489.
MLA Handbook (7th Edition):
Macara, Ann Marie. “Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits.” 2016. Web. 19 Jan 2020.
Vancouver:
Macara AM. Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits. [Internet] [Doctoral dissertation]. University of Michigan; 2016. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/133489.
Council of Science Editors:
Macara AM. Mechanisms that Underlie Experience-dependent Assembly of Neural Circuits. [Doctoral Dissertation]. University of Michigan; 2016. Available from: http://hdl.handle.net/2027.42/133489
University of California – Riverside
16.
Han, Michael.
The piRNA System in Aedes aegypti.
Degree: Cell, Molecular and Developmental Biology, 2017, University of California – Riverside
URL: http://www.escholarship.org/uc/item/1tm484b2
► The aim of the research presented in this thesis is to examine the piRNA pathway in Aedes aegypti, with an emphasis on understanding the role…
(more)
▼ The aim of the research presented in this thesis is to examine the piRNA pathway in Aedes aegypti, with an emphasis on understanding the role of the pathway in the soma. Chapter one reviews the piRNA pathway’s role in transposon regulation as well as transposon-independent roles, such as sex-determination in Bombyx mori. In addition, preliminary research from the Atkinson laboratory showed an expansion in the number and expression domain of the PIWI family in Aedes aegypti compared to a model Dipteran organism, Drosophila melanogaster. Chapter two introduces research I performed that showed the somatic expression of an important PIWI gene, Ago 3, in somatic ovarian follicular cells and larval gastric caecum. Piwi 2 was found to have a germline localization. In addition, an Ago 3 RNAi knockdown line (M14) exhibited a phenotype of larval mortality. Chapter three focuses on a new, more stringent method of annotating piRNA clusters in Ae. aegypti from different types of mosquito sRNA libraries, including both somatic and germline tissue. Two fairly distinct sets of piRNA clusters were discovered, one in the soma and one in the germline. Somatic clusters produced piRNA against predominately gypsy elements; somatic piRNA bore strong U1 signatures but weaker A10 signatures, and also bore less hallmarks of the piRNA ping-pong amplification loop. In contrast, germline clusters produced piRNA against a more varied set of transposons, and germline piRNA had both strong U1 and A10 signatures. Germline libraries also had larger quantities of transposon-derived piRNA. Chapter four examines the effect of Ago 3 knockdown in mosquito larvae. Modest decreases in U1 and A10 signatures were seen in piRNA sequenced from Ago 3 knockdown mosquitoes; in addition, the relative percent of piRNA mapping against transposons declined from wild-type and control conditions. A global decrease in mRNA mapping to transposons was also detected. Together, these data show that somatic piRNAs exist in Ae. aegypti. These piRNA play a role in transposon defense, but based on comparison with germline piRNA, somatic piRNA may also play a role in different pathways, such as gene regulation or viral defense.
Subjects/Keywords: Molecular biology; Cellular biology; Developmental biology; Ago 3; piRNA; PIWI; RNAI
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APA ·
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APA (6th Edition):
Han, M. (2017). The piRNA System in Aedes aegypti. (Thesis). University of California – Riverside. Retrieved from http://www.escholarship.org/uc/item/1tm484b2
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Han, Michael. “The piRNA System in Aedes aegypti.” 2017. Thesis, University of California – Riverside. Accessed January 19, 2020.
http://www.escholarship.org/uc/item/1tm484b2.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Han, Michael. “The piRNA System in Aedes aegypti.” 2017. Web. 19 Jan 2020.
Vancouver:
Han M. The piRNA System in Aedes aegypti. [Internet] [Thesis]. University of California – Riverside; 2017. [cited 2020 Jan 19].
Available from: http://www.escholarship.org/uc/item/1tm484b2.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Han M. The piRNA System in Aedes aegypti. [Thesis]. University of California – Riverside; 2017. Available from: http://www.escholarship.org/uc/item/1tm484b2
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Francisco
17.
Samocha, Alexandr.
Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals.
Degree: Biomedical Sciences, 2018, University of California – San Francisco
URL: http://www.escholarship.org/uc/item/4rn233xf
► Mammary stem cells (MaSC) are a heterogeneous population that give rise to progenitor cells subsequently developing into differentiated cells. The exact mammary epithelial cell (MEC)…
(more)
▼ Mammary stem cells (MaSC) are a heterogeneous population that give rise to progenitor cells subsequently developing into differentiated cells. The exact mammary epithelial cell (MEC) hierarchy and particularly the signals that govern this hierarchy are largely unknown. Several studies have implied a role for EGFR signals in the mammary epithelium but the exact role that of EGFR (Epidermal Growth Factor Receptor) has remained rather elusive. Insights from a 3-D ex vivo model derived from human breast tissue and studies using a hypomorphic EGFR allele have put forth a model that the strength of EGFR signals may impact cell fate decisions in the mammary gland. We obtained recent evidence indicating that the Ras guanine nucleotide exchange factor (RasGEF) Rasgrp1 can dampen EGFR signals in epithelial cells.We demonstrate that RasGEF Rasgrp1 is expressed in mammary epithelium and use cleared fat pad approaches to reveal a previously unrecognized functional role for RasGRP1 in the mammary gland. These approaches involved the transplantation of mammary epithelial cells (MECs) from Rasgrp1-deficient animals and from mice with a single point mutation in Rasgrp1, the Rasgrp1Anaef model. Biochemically, loss of Rasgrp1 as well as the Rasgrp1Anaef point mutation resulted in increased EGF-induced Ras-effector kinase signaling. MECs showed increase activation of the ERK-, Akt-, and mTORC1-S6- kinase pathways upon EGF stimulation when the MECs were isolated from Rasgrp1-/- or the Rasgrp1Anaef females. Using a model cell line, Eph4, we demonstrated that Rasgrp1’s suppressive action depends on its catalytic activity. Functionally, Rasgrp1 perturbation led to shortened mammary ductal trees in mammary whole mounts, increases in numbers of proliferative terminal end buds (TEBs), and sustained proliferation of mammary ductal cells (with high phospho-Akt) in areas where proliferation has normally halted. Organoid assays to reveal that Rasgrp1 perturbation led to a gain-of- function EGF-driven phenotype. With WT MECs, EGF drove the formation of spheres in organoid assays. By contrast, EGF induced robust branching of Rasgrp1-/- and Rasgrp1Anaef MECs that could be prevented when EGFR inhibitors are added. Thus, Rasgrp1 critically controls the mammary morphogenetic program as indicated by elevated branching morphogenesis upon EGF-EGFR signaling in the absence of Rasgrp1 function. MEC colony assays using Rasgrp1-/- and Rasgrp1Anaef cells revealed that progenitors form more and larger colonies than WT counterparts and with increased proliferation (Ki67) in response to EGF and strong staining for pAkt, all of which were reduced with EGFR inhibitors in the assays. Lastly, capitalizing on FACS profiling of mammary epithelial cells we established that Rasgrp1 perturbation led to alterations in cell fate of stem- and progenitor-cells in the mammary gland. Rasgrp1-/- and Rasgrp1Anaef mammary glands revealed decreased total cellularity of CD31-/CD45-/Ter119- lineage-negative cells but increased luminal CD49fmedium/EpCAMhigh and basal…
Subjects/Keywords: Developmental biology; Cellular biology; Molecular biology; development; epithelium; mammary; Ras; Rasgrp1
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APA (6th Edition):
Samocha, A. (2018). Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/4rn233xf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Samocha, Alexandr. “Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals.” 2018. Thesis, University of California – San Francisco. Accessed January 19, 2020.
http://www.escholarship.org/uc/item/4rn233xf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Samocha, Alexandr. “Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals.” 2018. Web. 19 Jan 2020.
Vancouver:
Samocha A. Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals. [Internet] [Thesis]. University of California – San Francisco; 2018. [cited 2020 Jan 19].
Available from: http://www.escholarship.org/uc/item/4rn233xf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Samocha A. Mammary Epithelial Cell Fate & EGFR-Rasgrp1-Ras Effector Signals. [Thesis]. University of California – San Francisco; 2018. Available from: http://www.escholarship.org/uc/item/4rn233xf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Arkansas
18.
Wadsworth, Benjamin.
The Functional Conservation of Frazzled in Insects.
Degree: MS, 2019, University of Arkansas
URL: https://scholarworks.uark.edu/etd/3387
► Axons in the developing embryo receive and react to signals that direct their growth to reach target tissues at specified locations. The signal pathways…
(more)
▼ Axons in the developing embryo receive and react to signals that direct their growth to reach target tissues at specified locations. The signal pathways that direct midline crossing of axons during embryonic development have been comprehensively examined in the past years using the Drosophila ventral nerve cord or the spinal cord as a model system. A number of these signaling mechanisms are conserved, however disparities have been found between species in general strategy or the
molecular signals controlling the response of axons to guidance cues.
The Netrin-Frazzled pathway has been shown to aid in midline crossing of axons in the embryonic ventral nerve cord of Drosophila. However, It is uncertain if this function of Frazzled is conserved in other insects. The goals of this research are to gain insight into the evolutionary conservation of axon guidance by the Netrin receptor Frazzled (Fra)and to expand our understanding of how Frazzled affects midline crossing in the flour beetle Triboliumcastaneum.
The Frazzled ortholog in Tribolim is sufficient for replacing loss of function in Drosophila Fra. We also expect to see similar expression and function of Frazzled in beetles to those observed in Drosophila. These studies expand our knowledge of axon guidance of midline crossing in a species that does not share some of Drosophila’s derived guidance characters. Using Tribolium as an insect model for comparative studies of axon guidance may allow us to see a more ancestral guidance scheme.
Advisors/Committee Members: Timothy Evans, Allen Szalanski, Nagayasu Nakanishi.
Subjects/Keywords: Cell Biology; Developmental Biology; Entomology; Integrative Biology; Molecular and Cellular Neuroscience
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APA (6th Edition):
Wadsworth, B. (2019). The Functional Conservation of Frazzled in Insects. (Masters Thesis). University of Arkansas. Retrieved from https://scholarworks.uark.edu/etd/3387
Chicago Manual of Style (16th Edition):
Wadsworth, Benjamin. “The Functional Conservation of Frazzled in Insects.” 2019. Masters Thesis, University of Arkansas. Accessed January 19, 2020.
https://scholarworks.uark.edu/etd/3387.
MLA Handbook (7th Edition):
Wadsworth, Benjamin. “The Functional Conservation of Frazzled in Insects.” 2019. Web. 19 Jan 2020.
Vancouver:
Wadsworth B. The Functional Conservation of Frazzled in Insects. [Internet] [Masters thesis]. University of Arkansas; 2019. [cited 2020 Jan 19].
Available from: https://scholarworks.uark.edu/etd/3387.
Council of Science Editors:
Wadsworth B. The Functional Conservation of Frazzled in Insects. [Masters Thesis]. University of Arkansas; 2019. Available from: https://scholarworks.uark.edu/etd/3387
University of Washington
19.
Peters, Nathaniel Clement.
From Transcription to Tubulogenesis: Insights from the Drosophila Ovary.
Degree: PhD, 2015, University of Washington
URL: http://hdl.handle.net/1773/34064
► During Drosophila melanogaster oogenesis, subsets of the epithelial cells that surround each developing egg chamber undergo morphogenesis to form epithelial tubes, and the lumens of…
(more)
▼ During Drosophila melanogaster oogenesis, subsets of the epithelial cells that surround each developing egg chamber undergo morphogenesis to form epithelial tubes, and the lumens of these tubes serve as molds for the dorsal appendage (DA) filaments of the mature eggshell. This process is a simple and tractable system for identifying and characterizing the
cellular events and
molecular mechanisms required for epithelial tube morphogenesis, or tubulogenesis. The work presented in this dissertation provides insight both into the upstream gene regulatory elements that set the stage and maintain control, and into the downstream
molecular effectors that govern cell shape, order, and movement, throughout DA tubulogenesis. In Chapter I, I highlight the fundamental importance of
cellular tubes and the intimate relationship between tube morphology and function, explain what we do and do not know about the
cellular and
molecular mechanisms that drive tubulogenesis, provide a detailed description of the process of DA tubulogenesis, and emphasize the advantages of DA tubulogenesis as a model for epithelial tubulogenesis. In Chapter II, I establish regulatory links, specifically in regard to DA tubulogenesis, between upstream transcription factors, such as Tramtrack69 and Mirror, and downstream effectors, such as Paxillin and Dynamin. In Chapter III, I focus specifically on the role of Dynamin and Dynamin-mediated endocytosis in DA tubulogenesis. I identify and characterize novel roles for Dynamin in epithelial tube closure, cell intercalation, and biased apical-luminal expansion. Furthermore, I provide evidence that Dynamin is regulating the levels and behavior of both E-Cadherin and Integrin-based
cellular adhesions, and propose that Dynamin facilitates the aforementioned
cellular, tubulogenic processes by regulating the turnover of
cellular adhesions. Finally, in Chapter IV, I summarize the results of my graduate research, discuss how these results fit with and augment our current knowledge of epithelial tubulogenesis, and propose future experiments that would further delve into the specific roles and mechanisms by which conserved, downstream, tubulogenic effectors, such as Dynamin and Paxillin, drive epithelial tubulogenesis.
Advisors/Committee Members: Berg, Celeste A (advisor).
Subjects/Keywords: Drosophila; Dynamin; Epithelium; Morphogenesis; Transcription; Tubulogenesis; Developmental biology; Genetics; Cellular biology; molecular and cellular biology
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APA (6th Edition):
Peters, N. C. (2015). From Transcription to Tubulogenesis: Insights from the Drosophila Ovary. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/34064
Chicago Manual of Style (16th Edition):
Peters, Nathaniel Clement. “From Transcription to Tubulogenesis: Insights from the Drosophila Ovary.” 2015. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/34064.
MLA Handbook (7th Edition):
Peters, Nathaniel Clement. “From Transcription to Tubulogenesis: Insights from the Drosophila Ovary.” 2015. Web. 19 Jan 2020.
Vancouver:
Peters NC. From Transcription to Tubulogenesis: Insights from the Drosophila Ovary. [Internet] [Doctoral dissertation]. University of Washington; 2015. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/34064.
Council of Science Editors:
Peters NC. From Transcription to Tubulogenesis: Insights from the Drosophila Ovary. [Doctoral Dissertation]. University of Washington; 2015. Available from: http://hdl.handle.net/1773/34064
Cal Poly
20.
Strand, Laura Therese.
A Proteomic Analysis of Differentiation in the Mammary Epithelium.
Degree: MS, Animal Science, 2012, Cal Poly
URL: https://digitalcommons.calpoly.edu/theses/825
;
10.15368/theses.2012.141
► While a great deal is known about the changing hormonal environment and the structural development of the mammary gland from pregnancy to lactation, very…
(more)
▼ While a great deal is known about the changing hormonal environment and the structural development of the mammary gland from pregnancy to lactation, very little is known about the
molecular mechanisms governing differentiation of the mammary epithelium into a milk-secreting phenotype. It is important to acknowledge the diversity among the mammary glands of different species in order to better understand applications in human health and the dairy industry. In this study, we examined global protein expression during two states of differentiation in mammary epithelial cells from two species: in vitro proliferating and differentiated MAC-T cells (a bovine immortal cell-line), and primary mammary epithelial cells isolated from pregnant and lactating mice. When comparing the lists of proteins that differed in abundance in the two experiments, we observed many similarities in proteins related to structural dynamics and mRNA processing within these two mammary epithelial cell types. Intriguingly, we observed several differences in the regulation of metabolic proteins, highlighting the distinct pathways by which different species probably metabolize energy and synthesize milk components.
Advisors/Committee Members: Daniel Gunnar Peterson.
Subjects/Keywords: Mammary; Mammary Development; Developmental Biology; Cellular Differentiation; Epithelial Differentiation; Molecular Biology
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APA (6th Edition):
Strand, L. T. (2012). A Proteomic Analysis of Differentiation in the Mammary Epithelium. (Masters Thesis). Cal Poly. Retrieved from https://digitalcommons.calpoly.edu/theses/825 ; 10.15368/theses.2012.141
Chicago Manual of Style (16th Edition):
Strand, Laura Therese. “A Proteomic Analysis of Differentiation in the Mammary Epithelium.” 2012. Masters Thesis, Cal Poly. Accessed January 19, 2020.
https://digitalcommons.calpoly.edu/theses/825 ; 10.15368/theses.2012.141.
MLA Handbook (7th Edition):
Strand, Laura Therese. “A Proteomic Analysis of Differentiation in the Mammary Epithelium.” 2012. Web. 19 Jan 2020.
Vancouver:
Strand LT. A Proteomic Analysis of Differentiation in the Mammary Epithelium. [Internet] [Masters thesis]. Cal Poly; 2012. [cited 2020 Jan 19].
Available from: https://digitalcommons.calpoly.edu/theses/825 ; 10.15368/theses.2012.141.
Council of Science Editors:
Strand LT. A Proteomic Analysis of Differentiation in the Mammary Epithelium. [Masters Thesis]. Cal Poly; 2012. Available from: https://digitalcommons.calpoly.edu/theses/825 ; 10.15368/theses.2012.141
University of Michigan
21.
Yang, Heiko.
A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis.
Degree: PhD, Cellular and Molecular Biology, 2016, University of Michigan
URL: http://hdl.handle.net/2027.42/120666
► How tissues adapt to varying nutrient conditions is of fundamental importance for robust tissue homeostasis throughout an organism’s lifespan, but the underlying mechanisms are poorly…
(more)
▼ How tissues adapt to varying nutrient conditions is of fundamental importance for robust tissue homeostasis throughout an organism’s lifespan, but the underlying mechanisms are poorly understood. Here we show that Drosophila testis responds to protein starvation by eliminating transit-amplifying spermatogonia (SGs) while maintaining a reduced pool of actively proliferating germline stem cells (GSCs). During protein starvation, SGs die in a manner that is mediated by the apoptosis of somatic cyst cells (CCs) that encapsulate SGs and regulate their development. Strikingly, GSCs cannot be maintained during protein starvation when CC-mediated SG death is inhibited, leading to an irreversible collapse of tissue homeostasis. SG death is associated with phagocytic processes that may directly promote GSC function via local nutrient recycling. We propose that the regulated elimination of transit-amplifying cells is essential to preserve stem cell function and tissue homeostasis during protein starvation.
Advisors/Committee Members: Yamashita, Yukiko (committee member), Lee, Cheng-Yu (committee member), Maillard, Ivan Patrick (committee member), Weisman, Lois S. (committee member), Joglekar, Ajit Prakash (committee member).
Subjects/Keywords: tissue homeostasis; stem cell biology; Molecular, Cellular and Developmental Biology; Science
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APA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Yang, H. (2016). A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/120666
Chicago Manual of Style (16th Edition):
Yang, Heiko. “A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis.” 2016. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/120666.
MLA Handbook (7th Edition):
Yang, Heiko. “A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis.” 2016. Web. 19 Jan 2020.
Vancouver:
Yang H. A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis. [Internet] [Doctoral dissertation]. University of Michigan; 2016. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/120666.
Council of Science Editors:
Yang H. A Modest Proposal: Differentiating Daughters are Sacrificed during Starvation to Protect Stem Cells in the Drosophila Testis. [Doctoral Dissertation]. University of Michigan; 2016. Available from: http://hdl.handle.net/2027.42/120666
University of Michigan
22.
Linsley, Jeremy William.
Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy.
Degree: PhD, Cellular & Molecular Biology, 2013, University of Michigan
URL: http://hdl.handle.net/2027.42/102419
► Excitation-contraction (EC) coupling is the mechanism by which muscle translates depolarization of the sarcolemma into Ca2+ release from the sarcoplasmic reticulum (SR) required for muscle…
(more)
▼ Excitation-contraction (EC) coupling is the mechanism by which muscle translates depolarization of the sarcolemma into Ca2+ release from the sarcoplasmic reticulum (SR) required for muscle contraction. EC coupling occurs at the junctions of transverse (t) tubules and SR called triads and is dependent on interactions between the dihydropyridine receptor (DHPR) in t-tubules that is the voltage detector, and the ryanodine receptor (RyR1) in the SR that is the Ca2+ release channel. Despite the well-studied role in EC coupling of DHPR and RyR1, other components of the
molecular complex are less understood. A mutagenesis screen of zebrafish identified an autosomal, recessive mutation that causes poor mobility and reduced Ca2+ release in skeletal muscle, yet exhibits normal output from the central nervous system to muscles. Through meiotic mapping, a null mutation in stac3, a skeletal muscle-specific gene encoding a putative adaptor protein, was identified. As stac3 mutants display myopathic features, we explored whether stac3 mutations might cause human myopathies and found that a mutation in STAC3 is the basis of Native American Myopathy, which is characterized by muscle weakness and susceptibility to malignant hyperthermia. The Stac3 protein was further characterized and found to directly interact with the EC coupling complex, and to function in normal trafficking and arrangement of the DHPR in arrays of four called tetrads that are essential for Ca2+ release.
The neuronally expressed Stac1 protein is a homolog of Stac3, but its function is unknown. Informed by our research on Stac3 in skeletal muscle, we probed the function of Stac1 in neurons. We find stac1 is expressed in a subset of spinal cord neurons in zebrafish embryos called Kolmer-Agdur (KA) interneurons that are likely involved in the neuronal circuit that generates swim behaviors. To determine the function of Stac1, we knocked down expression of Stac1 protein with an antisense morpholino oligonucleotide (MO), which resulted in a motility defect in embryos, indicating KA interneurons are involved in the neuronal circuit underlying swim behavior, and Stac1 is required swimming. These results indicate that members of the previously uncharacterized stac family of genes are important in normal muscle and neuronal physiology.
Advisors/Committee Members: Kuwada, John Y. (committee member), Xu, Haoxing (committee member), Isom, Lori L. (committee member), Hume, Richard I. (committee member), Barald, Katharine Francesca (committee member).
Subjects/Keywords: Cellular and Molecular Physiology of Skeletal Muscle and Neurons; Molecular, Cellular and Developmental Biology; Science
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APA ·
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CSE |
Export
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APA (6th Edition):
Linsley, J. W. (2013). Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/102419
Chicago Manual of Style (16th Edition):
Linsley, Jeremy William. “Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy.” 2013. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/102419.
MLA Handbook (7th Edition):
Linsley, Jeremy William. “Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy.” 2013. Web. 19 Jan 2020.
Vancouver:
Linsley JW. Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy. [Internet] [Doctoral dissertation]. University of Michigan; 2013. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/102419.
Council of Science Editors:
Linsley JW. Stac3 is a Component of the Excitation-Contraction Coupling Machinery and is Mutated in Native American Myopathy. [Doctoral Dissertation]. University of Michigan; 2013. Available from: http://hdl.handle.net/2027.42/102419
Iowa State University
23.
Solin, Staci Lyn.
Modeling pediatric brain and central nervous system cancer in zebrafish.
Degree: 2015, Iowa State University
URL: https://lib.dr.iastate.edu/etd/14910
► Brain and central nervous system (CNS) cancers are the leading cause of cancer-related death in children (Ostrom QT et al., 2015). Low-grade brain and CNS…
(more)
▼ Brain and central nervous system (CNS) cancers are the leading cause of cancer-related death in children (Ostrom QT et al., 2015). Low-grade brain and CNS tumors that require minimal surgical resection due to their location in critical regions are associated with long-term morbidity throughout the life of the child (Armstrong GT et al., 2011). Children diagnosed with high-grade, aggressive brain and CNS tumors generally have a poor outcome and suffer significant deficits in neurological and neuroendocrine function as a result of intensive therapy (Fangusaro J et al., 2012). Effective, targeted therapeutics for the treatment of pediatric brain and CNS cancer are needed. Gaining a better understanding of the molecular mechanisms underlying pediatric brain and CNS cancer initiation and progression will benefit the development of therapeutics. Animal models are an important component for the improvement of our understanding of the biology of these cancers (Huszthy PC et al., 2012). The zebrafish has recently emerged as a system for modeling human diseases including brain and CNS cancers. We have characterized two distinct zebrafish brain and CNS tumor models, a low-grade, glial-like tumor model and a high-grade CNS primitive neuroectodermal-like tumor model. The transgenic Tg(flk1:RFP)is18 zebrafish line develops low-grade glial-like tumors in the optic pathway including the retina, optic nerve and optic tract. These tumors exhibited histological features similar to those observed in human pediatric pilocytic astrocytoma. Differential gene expression analysis revealed a neuroglial progenitor signature in the tumors of the retina. The second brain tumor model helped establish the use of nuclease-mediated somatic mutagenesis in zebrafish for the study of tumor suppressor function in cancer. In this model we generated genetic mosaic adults using TALENs targeting the rb1 (retinoblastoma1) tumor suppressor. These mosaic adults developed predominantly undifferentiated, primitive neuroectodermal tumors (67% of tumors) as well as differentiated, glial-like tumors (33% of tumors). This was the first demonstration that somatic inactivation of a tumor suppressor causes cancer in zebrafish and highlighted the utility of site-specific nucleases as a rapid, simple, and cost efficient method to screen potentially hundreds of candidate tumor suppressor genes that impact tumorigenesis. These models will be useful for the study of pediatric brain and CNS tumorigenesis.
Subjects/Keywords: Molecular, Cellular and Developmental Biology; Brain cancer; RB Pathway; Zebrafish; Cell Biology; Molecular Biology
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APA (6th Edition):
Solin, S. L. (2015). Modeling pediatric brain and central nervous system cancer in zebrafish. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/14910
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Solin, Staci Lyn. “Modeling pediatric brain and central nervous system cancer in zebrafish.” 2015. Thesis, Iowa State University. Accessed January 19, 2020.
https://lib.dr.iastate.edu/etd/14910.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Solin, Staci Lyn. “Modeling pediatric brain and central nervous system cancer in zebrafish.” 2015. Web. 19 Jan 2020.
Vancouver:
Solin SL. Modeling pediatric brain and central nervous system cancer in zebrafish. [Internet] [Thesis]. Iowa State University; 2015. [cited 2020 Jan 19].
Available from: https://lib.dr.iastate.edu/etd/14910.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Solin SL. Modeling pediatric brain and central nervous system cancer in zebrafish. [Thesis]. Iowa State University; 2015. Available from: https://lib.dr.iastate.edu/etd/14910
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Washington
24.
Cruz, Ivan Alberto.
Adult Zebrafish Lateral Line: A Well Supported System.
Degree: PhD, 2015, University of Washington
URL: http://hdl.handle.net/1773/34063
► Hair cells are required for hearing and balance. Hair cell death is caused by multiple environmental insults, such as prolong exposure to loud noises, aminoglycoside…
(more)
▼ Hair cells are required for hearing and balance. Hair cell death is caused by multiple environmental insults, such as prolong exposure to loud noises, aminoglycoside antibiotics, some chemotherapeutics, and heavy metals, and hair cell loss is irreversible in humans. However, many other vertebrates such as, birds, fish and amphibians have the ability to replaced lost hair cells. Zebrafish has quickly become an excellent modeled to study hair cell
biology. Aside from the hair cells found in the inner ear, zebrafish have externally located hair cells on the head and body that allow them to detect changes in water currents. Also, larval zebrafish can quickly regenerate lost hair cells after traumatic damage. How hair cell precursors are replenished or maintained throughout the animal’s life is still unknown. I investigated lateral line hair cell and support cell maintenance in adult zebrafish, in which growth is largely complete. I demonstrate that adult zebrafish not only replenish hair cells after a single instance of hair cell damage, but also maintain hair cells and support cells after multiple rounds of damage and regeneration. I observed that hair cells undergo continuous turnover in adult zebrafish in the absence of damage. Mitotically-distinct support cell populations were identified and show that hair cells regenerate from underlying support cells in a region-specific manner. Using the transgenic Zebrabow-M fish line, I performed long-term multicolor clonal analysis to discover that lateral line neuromast drift towards clonality. However, I also observe that some neuromasts reach equilibrium and may indicate that multiple progenitors act to maintain the lateral line neuromast. Our results demonstrate that there are distinct support cell populations in the lateral line, which may help explain why zebrafish hair cell regeneration is extremely robust, retained throughout life, and potentially unlimited in regenerative capacity.
Advisors/Committee Members: Raible, David (advisor).
Subjects/Keywords: Lateral line system; Regeneration; Zebrafish; Developmental biology; Molecular biology; molecular and cellular biology
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APA (6th Edition):
Cruz, I. A. (2015). Adult Zebrafish Lateral Line: A Well Supported System. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/34063
Chicago Manual of Style (16th Edition):
Cruz, Ivan Alberto. “Adult Zebrafish Lateral Line: A Well Supported System.” 2015. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/34063.
MLA Handbook (7th Edition):
Cruz, Ivan Alberto. “Adult Zebrafish Lateral Line: A Well Supported System.” 2015. Web. 19 Jan 2020.
Vancouver:
Cruz IA. Adult Zebrafish Lateral Line: A Well Supported System. [Internet] [Doctoral dissertation]. University of Washington; 2015. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/34063.
Council of Science Editors:
Cruz IA. Adult Zebrafish Lateral Line: A Well Supported System. [Doctoral Dissertation]. University of Washington; 2015. Available from: http://hdl.handle.net/1773/34063
University of Washington
25.
Wilken, Matthew.
Elucidating the cis-regulatory landscape of retinal development and regeneration.
Degree: PhD, 2016, University of Washington
URL: http://hdl.handle.net/1773/36774
► The mammalian retina is a heterogeneous mix of neurons and one glial cell type that mediate photo-sensation. The mechanisms of its development and the generation…
(more)
▼ The mammalian retina is a heterogeneous mix of neurons and one glial cell type that mediate photo-sensation. The mechanisms of its development and the generation of cell type diversity is an area of on-going investigation. Unlike some lower vertebrates, mammalian retinas are largely incapable of regenerating lost neurons after retinal injury. In this work, I describe my efforts to map the cis-regulatory landscape of retinal development by employing DNase-hypersensitivity sequencing of retina at several important stages. The resulting data was categorized based on behavior to generate lists of putative cis-regulatory elements and transcription factors that regulate specific stages of retinal development. In addition, several putative enhancers were discovered for two key transcription factors, Otx2 and Ascl1. Next, we used this strategy to characterize the differences in cis-regulatory elements between retinal progenitors and cultured Muller glial cells. We found that the pro-neural transcription factor Ascl1, which is critical for retinal regeneration in the zebrafish, is able to partially reprogram mouse Muller glia into retinal neurons. Specifically, many retinal progenitor and neuronal genes were activated and the local chromatin environment was remodeled at ASCL1 binding sites. However, we found that ASCL1 binding within Muller glia only partially recapitulates the developmentally appropriate binding pattern found in retinal progenitors. Further, ASCL1 is able to bind to non-hypersensitive regions of chromatin in Muller glia. By comparing the accessible DNA of retinal progenitors and Muller glia, we were able to identify another factor, Zic1, which augments reprogramming. Finally, we show that perturbation of the epigenome during reprogramming, through the use of histone de-acetylase inhibitors, enhances reprogramming towards the photoreceptor cell fate. These results indicate that understanding the epigenetic state of cells can lead to insights into development and reprogramming with implications for regenerative medicine.
Advisors/Committee Members: Reh, Thomas A (advisor).
Subjects/Keywords: Ascl1; Glia; Regeneration; Reprogramming; Retina; Molecular biology; Developmental biology; molecular and cellular biology
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APA (6th Edition):
Wilken, M. (2016). Elucidating the cis-regulatory landscape of retinal development and regeneration. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/36774
Chicago Manual of Style (16th Edition):
Wilken, Matthew. “Elucidating the cis-regulatory landscape of retinal development and regeneration.” 2016. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/36774.
MLA Handbook (7th Edition):
Wilken, Matthew. “Elucidating the cis-regulatory landscape of retinal development and regeneration.” 2016. Web. 19 Jan 2020.
Vancouver:
Wilken M. Elucidating the cis-regulatory landscape of retinal development and regeneration. [Internet] [Doctoral dissertation]. University of Washington; 2016. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/36774.
Council of Science Editors:
Wilken M. Elucidating the cis-regulatory landscape of retinal development and regeneration. [Doctoral Dissertation]. University of Washington; 2016. Available from: http://hdl.handle.net/1773/36774
University of Washington
26.
Mathewson, Andrew Walter.
Dynamics of Planar Polarity in the Vertebrate Nervous System.
Degree: PhD, 2018, University of Washington
URL: http://hdl.handle.net/1773/40939
► The asymmetric localization of planar cell polarity (PCP) proteins is essential for the establishment of many planar polarized cellular processes, but the mechanisms that maintain…
(more)
▼ The asymmetric localization of planar cell polarity (PCP) proteins is essential for the establishment of many planar polarized
cellular processes, but the mechanisms that maintain these asymmetric distributions remain poorly understood. A body of evidence has tied oriented subapical microtubules (MTs) to the establishment of PCP protein polarity, yet recent studies have suggested that the MT cytoskeleton is later dispensable for the maintenance of this asymmetry. As MTs underlie the vesicular trafficking of membrane-bound proteins within cells, the requirement for MTs in the maintenance of PCP merited further investigation. I sought to investigate the complex interactions between PCP proteins and the MT cytoskeleton in the polarized context of the floorplate of the zebrafish neural tube. We demonstrated that the progressive posterior polarization of the primary cilia of floorplate cells requires not only Vangl2 but also Fzd3a. I determined that GFP-Vangl2 asymmetrically localizes to anterior membranes whereas Fzd3a-GFP is equally distributed on anterior and posterior membranes but maintains a cytosolic enrichment at the base of the primary cilium. Vesicular Fzd3a-GFP is rapidly trafficked along MTs primarily toward the apical membrane during a period of PCP maintenance, whereas GFP-Vangl2 appears to be less dynamic, maintaining asymmetry at the membrane. Nocodazole-induced loss of MT polymerization disrupts basal body positioning as well as GFP-Vangl2 localization and reduces cytosolic Fzd3a-GFP movements. Removal of nocodazole after MT disruption restores MT polymerization but does not restore basal body polarity. Interestingly, GFP-Vangl2 repolarizes to anterior membranes and Fzd3a-GFP largely re-establishes normal dynamics after multiple hours of recovery, even in the context of unpolarized basal bodies. Together my findings challenge previous work by revealing an ongoing role for MT-dependent transport of PCP proteins in maintaining both
cellular and PCP protein asymmetry during development. PCP signaling has been implicated in the directional migration of single cells during development, especially within the developing nervous system. One such migration is the tangential migration of facial branchiomotor neurons (FBMNs) in the highly polarized context of the vertebrate hindbrain. It is well-established that many core PCP and PCP-related signaling components are required for FBMN migration, yet how PCP signaling is used to enable this migration is not well understood. By systematically disrupting PCP signaling in a rhombomere-restricted manner we show that PCP signaling is required both within FBMNs and the hindbrain rhombomere 4 environment at the time when they initiate their migration. Correspondingly, we demonstrate planar polarized localization of PCP core components Vangl2 and Fzd3a in the hindbrain neuroepithelium, and transient localization of Vangl2 at the tips of retracting FBMN filopodia. Using high-resolution timelapse imaging of FBMNs in genetic chimeras we uncover opposing cell-autonomous and…
Advisors/Committee Members: Moens, Cecilia B (advisor).
Subjects/Keywords: Floorplate; Fzd3a; Neurons; Planar; Polarity; Vangl2; Developmental biology; Cellular biology; Molecular biology; Molecular and cellular biology
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APA ·
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MLA ·
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APA (6th Edition):
Mathewson, A. W. (2018). Dynamics of Planar Polarity in the Vertebrate Nervous System. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/40939
Chicago Manual of Style (16th Edition):
Mathewson, Andrew Walter. “Dynamics of Planar Polarity in the Vertebrate Nervous System.” 2018. Doctoral Dissertation, University of Washington. Accessed January 19, 2020.
http://hdl.handle.net/1773/40939.
MLA Handbook (7th Edition):
Mathewson, Andrew Walter. “Dynamics of Planar Polarity in the Vertebrate Nervous System.” 2018. Web. 19 Jan 2020.
Vancouver:
Mathewson AW. Dynamics of Planar Polarity in the Vertebrate Nervous System. [Internet] [Doctoral dissertation]. University of Washington; 2018. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/1773/40939.
Council of Science Editors:
Mathewson AW. Dynamics of Planar Polarity in the Vertebrate Nervous System. [Doctoral Dissertation]. University of Washington; 2018. Available from: http://hdl.handle.net/1773/40939
27.
Joseph, Giselle A.
The Role of Group I Paks in Postnatal Muscle Development and Homeostasis.
Degree: 2017, Icahn School of Medicine at Mount Sinai
URL: http://pqdtopen.proquest.com/#viewpdf?dispub=10640750
► Group I Paks are serine/threonine kinases that function as major effectors of the small GTPases Rac1 and Cdc42. They regulate many cellular functions, including…
(more)
▼ Group I Paks are serine/threonine kinases that function as major effectors of the small GTPases Rac1 and Cdc42. They regulate many cellular functions, including cell polarity, cytoskeletal dynamics, and transcription. Pak1 and Pak2 are redundantly essential for embryonic skeletal myoblast fusion in <i> Drosophila</i>, with Pak2 playing the more important role. Both are expressed in mammalian skeletal muscle, but little is known as to their function in myogenesis. We find that Pak1 and Pak2 are expressed in mammalian myoblasts and are activated specifically during differentiation. Individual genetic deletions of <i>Pak1</i> and <i>Pak2</i> in mice show no overt defects in muscle development or regeneration. However, young adult mice with muscle-specific deletion of <i>Pak1</i> and <i>Pak2 </i> together (dKO mice) present with reduced muscle mass and a higher proportion of myofibers with smaller cross-sectional area compared to controls. This phenotype is exacerbated after repair to acute injury. Primary myoblasts from dKO animals show delayed differentiation, with lower expression of myogenic markers and inefficient myotube formation. Additionally, with age, dKO mice develop a chronic myopathy. Histological analyses of resting muscle show the presence of central nuclei in the majority of fibers, as well as significant fibrosis, inflammation, necrosis, and hypertrophy with fiber splitting. Ultrastructural analysis revealed grossly elongated and branched intermyofibrillar mitochondria, known as megaconial mitochondria, along with occasional accumulation of subsarcolemmal mitochondria. Moreover, dKO mice show impaired mitochondrial function, with significantly reduced Complex I and II activity. These characteristics are absent in control animals. We conclude that the role of Pak1 and Pak2 in embryonic myoblast fusion, first identified in the fly, is not conserved in mammals. Rather, our data demonstrate that Pak1 and Pak2 function redundantly in regulating myoblast differentiation, thereby impacting overall postnatal muscle size. Furthermore, their major function appears to be in muscle homeostasis. Few protein kinases have been implicated in muscle disease. Group I Paks have wide roles in cell regulation, and the generation of dKO mice provides a genetic system to gain new mechanistic insights into muscle maintenance, as well as to discover the substrates of Paks that regulate this process.
Subjects/Keywords: Biology; Cellular biology; Developmental biology
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APA ·
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MLA ·
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APA (6th Edition):
Joseph, G. A. (2017). The Role of Group I Paks in Postnatal Muscle Development and Homeostasis. (Thesis). Icahn School of Medicine at Mount Sinai. Retrieved from http://pqdtopen.proquest.com/#viewpdf?dispub=10640750
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Joseph, Giselle A. “The Role of Group I Paks in Postnatal Muscle Development and Homeostasis.” 2017. Thesis, Icahn School of Medicine at Mount Sinai. Accessed January 19, 2020.
http://pqdtopen.proquest.com/#viewpdf?dispub=10640750.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Joseph, Giselle A. “The Role of Group I Paks in Postnatal Muscle Development and Homeostasis.” 2017. Web. 19 Jan 2020.
Vancouver:
Joseph GA. The Role of Group I Paks in Postnatal Muscle Development and Homeostasis. [Internet] [Thesis]. Icahn School of Medicine at Mount Sinai; 2017. [cited 2020 Jan 19].
Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10640750.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Joseph GA. The Role of Group I Paks in Postnatal Muscle Development and Homeostasis. [Thesis]. Icahn School of Medicine at Mount Sinai; 2017. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10640750
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – Santa Cruz
28.
Smith, Prestina.
Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development.
Degree: Molecular Cell and Developmental Biology, 2017, University of California – Santa Cruz
URL: http://www.escholarship.org/uc/item/8sj0c19q
► The breast (mammary gland) is a dynamic organ that undergoes multiple stages of expansion during puberty and pregnancy. During pubertal growth, the mammary gland undergoes…
(more)
▼ The breast (mammary gland) is a dynamic organ that undergoes multiple stages of expansion during puberty and pregnancy. During pubertal growth, the mammary gland undergoes branching morphogenesis to generate a bilayered-branched epithelium. Driving branching morphogenesis are extracellular cues that regulate cell proliferation and tissue expansion. The WNT superfamily of secreted signaling molecules governs many of the developmental processes that occur during mammary gland morphogenesis through interactions with specific receptors. While canonical WNT receptors have been investigated in the mammary gland, the role of receptors that function solely in non-canonical WNT signaling remain elusive. In Chapter 1, I review current knowledge of extracellular cues that regulate asymmetric cell division, an important aspect of development. Next, I show that non-canonical WNT receptors ROR2 and VANGL2 regulate branching and proliferation of the mammary gland. In the first study, I characterize Ror2-/- mice and perform serial transplantation experiments that reveal hyperbranching and tissue longevity phenotypes. In vivo experiments in which WT and Ror2-/- mammary outgrowths are exposed to exogenous WNT5A signals reveal that ROR2 is required for restricting the process of branching morphogenesis. In a second study, I show that the non-canonical WNT/Planar cell polarity protein VANGL2 regulates multiple types of growth in the mammary gland. Mammary reconstitution assays, in which I transplanted fragments of WT or VANGL2 mutant tissue into mammary fat pads that have their endogenous epithelia removed, revealed that loss of VANGL2 function generates smaller mammary outgrowths compared to WT. These mutants also display defects in branching. Using lentiviral- mediated knockdown of Vangl2 in cultured primary mammary epithelial cells, I stratified the function of VANGL2 by cell-type. Lastly, I found that loss of VANGL2 function leads to down regulation of the transcriptional repressor Bmi1. Together, the studies provide insight into the mechanisms that drive morphogenesis during mammary gland development.
Subjects/Keywords: Biology; Cellular biology; Developmental biology
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APA ·
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MLA ·
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CSE |
Export
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APA (6th Edition):
Smith, P. (2017). Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development. (Thesis). University of California – Santa Cruz. Retrieved from http://www.escholarship.org/uc/item/8sj0c19q
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Smith, Prestina. “Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development.” 2017. Thesis, University of California – Santa Cruz. Accessed January 19, 2020.
http://www.escholarship.org/uc/item/8sj0c19q.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Smith, Prestina. “Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development.” 2017. Web. 19 Jan 2020.
Vancouver:
Smith P. Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development. [Internet] [Thesis]. University of California – Santa Cruz; 2017. [cited 2020 Jan 19].
Available from: http://www.escholarship.org/uc/item/8sj0c19q.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Smith P. Non-canonical WNT signaling through ROR2 and VANGL2 in mammary gland development. [Thesis]. University of California – Santa Cruz; 2017. Available from: http://www.escholarship.org/uc/item/8sj0c19q
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Diego
29.
Lakoduk, Ashley Marie.
Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis.
Degree: Biology, 2012, University of California – San Diego
URL: http://www.escholarship.org/uc/item/2gh3w4sn
► In a study by Charest et al., 2010 a protein signaling complex was discovered and found to regulate the RasC-TORC-PKB/PKBR1 pathway at the leading edge…
(more)
▼ In a study by Charest et al., 2010 a protein signaling complex was discovered and found to regulate the RasC-TORC-PKB/PKBR1 pathway at the leading edge of chemotaxing Dictyostelium discoideum cells. A novel protein, PHR, is a stable member of this Sca1 protein complex. This present study is an in-depth analysis of phr null strains in the regulation of chemotaxis in Dictyostelium cells. Analyses of phr knockout cells show clear alteration of actin and myosin cytoskeleton dynamics as well as altered cell motility. Though it was discovered that PHR is a stable member of the Sca1 protein signaling complex, it does not affect RasC activity. Intriguingly, phr knockout does seem to modulate the downstream TORC2-mediated phosphorylation of PKB and PKBR1 proteins, despite having no observed effect on RasC activity. Thus, additional roles for PHR in regulating chemotaxis outside of the Sca1 complex was proposed. However, due to the fact that the correct topology of the PHR gene is currently unknown, attempts to generate cells expressing epitope-tagged PHR to test for alternative roles in chemotaxis regulation has proven unsuccessful. The exact functions of PHR in the spatiotemporal regulation of chemotaxis remains unclear.
Subjects/Keywords: Biology; Developmental biology; Cellular biology
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APA ·
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Export
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APA (6th Edition):
Lakoduk, A. M. (2012). Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/2gh3w4sn
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lakoduk, Ashley Marie. “Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis.” 2012. Thesis, University of California – San Diego. Accessed January 19, 2020.
http://www.escholarship.org/uc/item/2gh3w4sn.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lakoduk, Ashley Marie. “Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis.” 2012. Web. 19 Jan 2020.
Vancouver:
Lakoduk AM. Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis. [Internet] [Thesis]. University of California – San Diego; 2012. [cited 2020 Jan 19].
Available from: http://www.escholarship.org/uc/item/2gh3w4sn.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lakoduk AM. Investigation into the function of a novel protein, PHR, in regulating Dictyostelium discoideum chemotaxis. [Thesis]. University of California – San Diego; 2012. Available from: http://www.escholarship.org/uc/item/2gh3w4sn
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Michigan
30.
Norris, Stephen R.
A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells.
Degree: PhD, Biophysics, 2014, University of Michigan
URL: http://hdl.handle.net/2027.42/110504
► Collective motor dynamics drives important cellular processes ranging from muscle contraction to spindle organization to vesicle trafficking (Chapter 1). Although the biomechanical and biochemical properties…
(more)
▼ Collective motor dynamics drives important
cellular processes ranging from muscle contraction to spindle organization to vesicle trafficking (Chapter 1). Although the biomechanical and biochemical properties of individual motors have been widely studied, how motors coordinate their motility when attached to the same cargo is largely unknown.
In this dissertation, I present a synthetic
biology technique (Chapter 2) to generate multi-motor assemblies whose biological properties can be examined in vitro and in living cells. To do this, we assembled a “toolbox” of protein components consisting of scaffolds and linkers. We characterized scaffold proteins of different lengths that allow for specific separation distances between the components. We then characterized four different linker systems that enable constitutive or regulated attachment of individual motors to scaffolds. We then showed, through FRET and subcellular localization experiments, that this toolbox could be used to generate defined assemblies in living cells.
Next, I present a characterization of fluorescent tags for use in single-molecule experiments (Chapter 3), and show that certain tags lead to aberrant kinesin-1 run lengths due to oligomerization. This study will provide a valuable reference for the field in choosing proper fluorescent tags for single-molecule experiments.
I then present a series of experiments where we use this system to investigate the behavior of two motors attached to a scaffold (Chapter 4). We find that two kinesin motors in complex act independently (do not help or hinder each other) and can alternate their activities. For complexes containing a slow kinesin-1 and fast kinesin-3 motor, the slow motor dominates motility in vitro but the fast motor can dominate on certain subpopulations of microtubules in cells. Both motors showed dynamic interactions with the complex, suggesting that motor-cargo linkages are sensitive to forces applied by the motors. We conclude that kinesin motors in complex act independently in a manner regulated by the microtubule track.
Overall, the approach presented in this dissertation is applicable to other biological questions such as the generation of complex signaling networks as well as the assembly of artificial biological systems for engineering applications (Chapter 5).
Advisors/Committee Members: Verhey, Kristen J. (committee member), Sept, David Samuel (committee member), Cai, Dawen (committee member), Liu, Allen Po-chih (committee member), Sivaramakrishnan, Sivaraj (committee member).
Subjects/Keywords: Synthetic Biology; Kinesin; Molecular Motors; Cytoskeleton; Biophysics; Molecular, Cellular and Developmental Biology; Science
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APA ·
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Export
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APA (6th Edition):
Norris, S. R. (2014). A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/110504
Chicago Manual of Style (16th Edition):
Norris, Stephen R. “A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells.” 2014. Doctoral Dissertation, University of Michigan. Accessed January 19, 2020.
http://hdl.handle.net/2027.42/110504.
MLA Handbook (7th Edition):
Norris, Stephen R. “A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells.” 2014. Web. 19 Jan 2020.
Vancouver:
Norris SR. A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells. [Internet] [Doctoral dissertation]. University of Michigan; 2014. [cited 2020 Jan 19].
Available from: http://hdl.handle.net/2027.42/110504.
Council of Science Editors:
Norris SR. A Novel Synthetic Biology Method to Study the Cooperative Behavior of Kinesin Motors in Cells. [Doctoral Dissertation]. University of Michigan; 2014. Available from: http://hdl.handle.net/2027.42/110504
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Open Access Theses and Dissertations
