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Rutgers University
1.
Tiger, Kumar Lee, 1991-.
glb-28's role in mating behavior and extracellular vesicle releasing neurons.
Degree: MS, glb-28, 2020, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64055/ 
► Genetic diseases arise from a mutation in a globin protein in humans in hemoglobinopathies, one of the most common diseases that can be inherited. The…
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▼ Genetic diseases arise from a mutation in a globin protein in humans in hemoglobinopathies, one of the most common diseases that can be inherited. The types of hemoglobinopathy range from structural hemoglobin variants to hemoglobin synthesis disorders. Globins in general are a conserved protein family that is characterized by its 6-8 alpha helices with an oxygen-interacting heme group and exist in all the kingdoms of life. The comprehensive study of globins are critical for more than just hemoglobin; they include myoglobin, neuroglobin, cytoglobin, androglobin, globin E, globin X, and globin Y in vertebrates. Neuroglobin, myoglobin, and cytoglobin have been studied the most out of the vertebrate globins. Caenorhabditis elegans globins offer the ability to understand globin protein function at a more fundamental level due to the large number and variety of globins, number of displayed phenotypes, sexual dimorphism, and ease of separating internal and external factors on protein function without inducing lethality. Despite these advantages, only 6 out of 34 globins have been characterized in the nematode C. elegans. It is still unknown why a nematode would have so many globins compared to more complex organisms which have fewer globins. I recently discovered that glb-28, one of the uncharacterized 34 globins of C. elegans, is endogenously expressed in extracellular vesicle-releasing neurons (EVNs) and oxygen sensing neurons. Currently, glb-28 is the only globin found in EVNs and it is required in male mating behavior. I will utilize CRISPR/Cas9 mediated genome editing to investigate the function of glb-28 in mating behavior, oxygen sensing neurons and EVNs. Results from this thesis may a novel connection with glb-28 between EVNs.
Advisors/Committee Members: Barr, Maureen M (chair), Singson, Andrew (co-chair), Langer, Jerome (co-chair), School of Graduate Studies.
Subjects/Keywords: Globin; Cell and Developmental Biology
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APA (6th Edition):
Tiger, Kumar Lee, 1. (2020). glb-28's role in mating behavior and extracellular vesicle releasing neurons. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64055/
Chicago Manual of Style (16th Edition):
Tiger, Kumar Lee, 1991-. “glb-28's role in mating behavior and extracellular vesicle releasing neurons.” 2020. Masters Thesis, Rutgers University. Accessed April 12, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/64055/.
MLA Handbook (7th Edition):
Tiger, Kumar Lee, 1991-. “glb-28's role in mating behavior and extracellular vesicle releasing neurons.” 2020. Web. 12 Apr 2021.
Vancouver:
Tiger, Kumar Lee 1. glb-28's role in mating behavior and extracellular vesicle releasing neurons. [Internet] [Masters thesis]. Rutgers University; 2020. [cited 2021 Apr 12].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64055/.
Council of Science Editors:
Tiger, Kumar Lee 1. glb-28's role in mating behavior and extracellular vesicle releasing neurons. [Masters Thesis]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64055/
Rutgers University
2.
Rodriguez-Colon, Lizahira, 1987-.
Role of G9a methyltransferase in the dna damage response signal.
Degree: PhD, Pharmacology, Cellular and Molecular, 2018, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/57687/
► DNA damage induces a choreographed set of local changes in histone modifications which leads to efficient recruitment of DNA repair factors. The regulation of these…
(more)
▼ DNA damage induces a choreographed set of local changes in histone modifications which leads to efficient recruitment of DNA repair factors. The regulation of these chromatin modifications at DNA breaks is critical to maintain genome integrity. Recent studies in our lab have identified a role for G9a methyltransferase in regulating DNA repair. The overall aim of this project was to elucidate how G9a activity regulates this pathway and to identify the effects of its inhibition in this process. It was shown that G9a localizes to sites of DNA damage in an ATM-dependent fashion and that inhibition of G9a activity affects early recruitment of multiple DNA repair factors. We found that catalytic inhibition of G9a using UNC0638 results in increased ATM activation. This led to increased "spreading" of pH2AX and MDC1 signals seen at regions of localized DNA breaks induced by UV-laser scissors, which was dependent upon ATM activation. This was also associated with increased levels of H3K36me2 and H3K56Ac. Biochemical data showed that G9a interacts and regulates HDAC1/2 activity during the DNA damage response. G9a inhibition led to decreased HDAC1 methylation, and increased ATM acetylation. These data suggest that G9a activity regulates the extent of ATM activation induced by DNA breaks and is required for efficient recruitment of downstream DNA repair factors. Overall our data suggests that G9a plays a critical role in regulation of ATM-dependent signaling during the DNA damage response and raises the possibility of using G9a inhibitors in the clinical setting as part of novel cancer therapies.
Advisors/Committee Members: Xia, Bing (chair), Pine, Sharon (internal member), Ganesan, Shridar (internal member), Langer, Jerome (outside member), School of Graduate Studies.
Subjects/Keywords: DNA repair
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APA (6th Edition):
Rodriguez-Colon, Lizahira, 1. (2018). Role of G9a methyltransferase in the dna damage response signal. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/57687/
Chicago Manual of Style (16th Edition):
Rodriguez-Colon, Lizahira, 1987-. “Role of G9a methyltransferase in the dna damage response signal.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 12, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/57687/.
MLA Handbook (7th Edition):
Rodriguez-Colon, Lizahira, 1987-. “Role of G9a methyltransferase in the dna damage response signal.” 2018. Web. 12 Apr 2021.
Vancouver:
Rodriguez-Colon, Lizahira 1. Role of G9a methyltransferase in the dna damage response signal. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 12].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57687/.
Council of Science Editors:
Rodriguez-Colon, Lizahira 1. Role of G9a methyltransferase in the dna damage response signal. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57687/
Rutgers University
3.
Ibironke, Olufunmilola, 1978-.
Air pollution particulate matter effects on adaptive human antimycobacterial immunity.
Degree: PhD, Physiology and Integrative Biology, 2019, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/
► Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies provide evidence that indoor (household) air pollution increases the…
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▼ Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies provide evidence that indoor (household) air pollution increases the risk of new infections with Mycobacterium tuberculosis (M.tb) and development of TB. The mechanisms by which exposure to ‘real-world’-derived urban ambient (outdoor) particulate matter (PM) adversely affects M.tb-specific human host T cell functions in vitro have not been studied. In this thesis research, we explored the effects of air pollution PM2.5 (≤2.5 µm, median aerodynamic diameter) collected in the Iztapalapa municipality of Mexico City on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). Upon in vitro exposure, PM2.5 was observed in clusters of free, non-membrane-bound particle agglomerates in the cytoplasm of the exposed cells. PM2.5 exposure did not alter the expression of activation marker CD54 on antigen presenting cells (APC), however, increased the expression of CD80 while decreasing the constitutively expressed CD86 on monocytes during M.tb infection. Exposure to PM2.5 of M.tb-infected PBMC led to an increase of intracellular growth of M.tb, indicating loss of M.tb growth controlling capacity of the cells that occurred independent of PM-induced changes to PBMC viability. Exposure of PBMC to PM2.5 also altered M.tb-specific T-cell immune responses by (1) decreasing the surface expression of early T cell activation markers CD69 and CD25 on T cells, (2) inhibiting the intracellular expression of both interferon-gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α), and (3) decreasing the expression of T-box transcription factor TBX21 (T-bet) known to directly regulate the expression of IFN-γ. In contrast, PM2.5 exposure increased the intracellular expression of the anti-inflammatory cytokine interleukin 10 (IL-10) and the phosphorylation of transcription factor STAT-3. The observed PM2.5-induced decrease in the expression of human pro-inflammatory M.tb-specific T cell cytokines, and the loss of intracellular M.tb growth control are associated with the increased expression of anti-inflammatory cytokine IL-10 and decreased expression of transcription factor T-bet. Together, the findings of this study suggest that the PM2.5-induced decrease of critical human host immune cell functions against M.tb represents the mechanistic correlate of epidemiological observations that outdoor air pollution exposure is associated with increases in the incidence of TB and with adversely modified TB treatment outcomes.
Advisors/Committee Members: Fan, Huizhou (chair), Langer, Jerome (internal member), Haimovich, Beatrice (internal member), Medina, Daniel (internal member), School of Graduate Studies.
Subjects/Keywords: Air – Pollution; Tuberculosis
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APA (6th Edition):
Ibironke, Olufunmilola, 1. (2019). Air pollution particulate matter effects on adaptive human antimycobacterial immunity. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60169/
Chicago Manual of Style (16th Edition):
Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 12, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.
MLA Handbook (7th Edition):
Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Web. 12 Apr 2021.
Vancouver:
Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 12].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.
Council of Science Editors:
Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/
Rutgers University
4.
Villegas, Gabriel.
Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster.
Degree: PhD, Biochemistry, 2020, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64889/
► D. melanogaster is an extremely powerful genetic animal model to study why and how we sleep. Like humans, the majority of sleep in D. melanogaster…
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▼ D. melanogaster is an extremely powerful genetic animal model to study why and how we sleep. Like humans, the majority of sleep in D. melanogaster occurs during the night. However, similar to many other day-active animals, D. melanogaster exhibits a midday sleep or “siesta”, most frequently associated with limiting exposure to the hot midday sun. Recent evidence indicates a strong genetic component influencing siesta behavior in humans. While nighttime and daytime sleep serve different functions, the role and mechanisms for siesta are little understood.
Initial studies from our laboratory showed that midday siesta in D. melanogaster is down-regulated by the cold-enhanced splicing of the 3’ terminal intron (termed dmpi8) in the period (per) gene, a key component of the circadian (~24 h) clock. More recent results revealed that dmpi8 splicing influences midday siesta in-trans via up-regulating the expression of a slightly overlapping gene termed daywake (dyw) that functions in an anti-siesta capacity. Overall, the main idea from prior work is that dyw mainly functions in thermal-adaptation whereby its increased levels on cool days reduces siesta levels by promoting midday wakefulness on days where the threat from heat exposure is diminished.
The dyw gene encodes a juvenile hormone binding protein (JHBP), which are known to be secreted into the hemolymph as part of signaling cascades. In this thesis I raised anti-DYW antibodies and used them to characterize the DYW protein at the biochemical and cellular levels in both flies and cultured Drosophila cells. DYW is found in key circadian cells in the brain, the pigment-dispersing factor (PDF)-expressing neurons, consistent with earlier work showing that manipulating dyw levels in these cells modulates midday siesta. DYW levels in the head are responsive to temperature and differ in male and female adult flies. There are two major isoforms of DYW in adult flies that appear to reflect post-translational differences. Indeed, studies in cultured Drosophila cells indicate that DYW stability and/or maturation is heavily dependent on a glycosylation event at a single residue position. Further, this work shows that DYW is secreted and that this secretion is reliant on the presence of an N-terminal signal peptide comprised of the first 25 residues in DYW. My studies suggest a model whereby DYW functions as a JHBP that is produced in the brain followed by cleavage and entry into the circulatory system where it interacts with target tissues to regulate sleep-wake behavior.
In related work, CRISPR technology was used to generate dyw knock-out (dyw-KO) flies. Remarkably, although dyw-KO flies exhibit increased midday sleep compared to wildtype controls as expected, when challenged with malnourishment we observe major differences in the regulation of nighttime sleep between dyw-KO flies and controls. This finding suggests that with prolonged hunger, dyw mainly stimulates wake during the night. Presumably, this helps in foraging for food but shifts this activity…
Advisors/Committee Members: Edery, Isaac (chair), Langer, Jerome (internal member), Belden, William J (internal member), Haimovich, Beatrice (outside member), School of Graduate Studies.
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APA (6th Edition):
Villegas, G. (2020). Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64889/
Chicago Manual of Style (16th Edition):
Villegas, Gabriel. “Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster.” 2020. Doctoral Dissertation, Rutgers University. Accessed April 12, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/64889/.
MLA Handbook (7th Edition):
Villegas, Gabriel. “Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster.” 2020. Web. 12 Apr 2021.
Vancouver:
Villegas G. Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster. [Internet] [Doctoral dissertation]. Rutgers University; 2020. [cited 2021 Apr 12].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64889/.
Council of Science Editors:
Villegas G. Biochemical and functional analysis of daywake, a novel wake-sleep regulator in drosophila melanogaster. [Doctoral Dissertation]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64889/
Rutgers University
5.
Laureano-Ruiz, Alejandra S.
The role of transcriptional elements during neuronal inner ear development.
Degree: PhD, Statoacoustic ganglion, 2021, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/65455/
► The integration of auditory and vestibular sensory inputs from our environment underlies our ability to hear, maintain spatial orientation, and balance. Otic mechanosensory cells (hair…
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▼ The integration of auditory and vestibular sensory inputs from our environment underlies our ability to hear, maintain spatial orientation, and balance. Otic mechanosensory cells (hair cells) and neurons are responsible for conveying and relaying sensory information to the brain. Inner ear disorders are often a result of mutations in transcription factors involved in the development of neurosensory progenitors that give rise to hair cells and otic neurons. The discovery and study of genetic factors that contribute to the development of the inner ear neurosensory cells will clarify the molecular etiology inner ear impairments and promote the advancement of strategies to treat inner ear disorders.
In this thesis, I have reviewed the key molecular mechanisms that drive inner ear development, morphology, and function. To study and identify transcription factors involved in otic neurosensory cell development, I utilized a fate restricted stem cell line of self-renewing immortalized multipotent otic progenitors (iMOPs). Under distinct culture conditions, iMOP cells can self-renew and maintain an otic progenitor state or differentiate into neurons that molecularly and morphologically resemble otic neurons. Furthermore, to holistically characterize the role of iMOP identified transcription factors during otic neurosensory development, I utilized the evolutionarily and functionally conserved inner ear of the embryonic zebrafish.
Using the iMOP cellular system, the role of SOX2 in otic neuron development was studied. A crucial milestone in otic neuronal development is the cell cycle exit of neuronal progenitor cells. Chromatin immunoprecipitation of SOX2 followed by sequencing of the pulled-down DNA fragments in proliferating iMOP (neurosensory progenitor-like cells) and iMOP-derived neurons showed SOX2 to be enriched in the promoter region of cell cycle inhibitors (e.g., Cdkn1b) in both cellular states. Furthermore, knockdown of SOX2 significantly reduced the expression of CDKN1B in iMOP derived neurons and prevented neuronal differentiation of iMOP cells. These experiments lead us to conclude that SOX2 is a critical regulator of otic neuron differentiation. SOX2 does this by regulating the expression of cell cycle inhibitors to promote a post-mitotic state, a critical stage in the progression of otic neuronal differentiation.
To further understand the molecular progression of otic neuronal differentiation, a pseudo time trajectory-based model of neuronal differentiation was generated using the iMOP cellular system. To build this model, TUBB3 labeled neurites from morphologically heterogeneous post-mitotic iMOP-derived neuron cultures were measured and clustered based on neurite length similarities. The neurite length of iMOP-derived neurons defined the differentiation state. The clustered neurites were arranged in an ascending manner. Fluorescence intensity of transcription factors critical for otic neuronal differentiation SOX2 and NEUROD1 was measured in pseudo time order iMOP-derived neurons. During early iMOP…
Advisors/Committee Members: Kwan, Kelvin Y (chair), Sabaawy, Hatem E (internal member), Millonig, James (internal member), Langer, Jerome A (outside member), School of Graduate Studies.
Subjects/Keywords: Labyrinth (Ear); Auditory pathways; Developmental neurobiology; Cell and Developmental Biology
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APA ·
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APA (6th Edition):
Laureano-Ruiz, A. S. (2021). The role of transcriptional elements during neuronal inner ear development. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/65455/
Chicago Manual of Style (16th Edition):
Laureano-Ruiz, Alejandra S. “The role of transcriptional elements during neuronal inner ear development.” 2021. Doctoral Dissertation, Rutgers University. Accessed April 12, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/65455/.
MLA Handbook (7th Edition):
Laureano-Ruiz, Alejandra S. “The role of transcriptional elements during neuronal inner ear development.” 2021. Web. 12 Apr 2021.
Vancouver:
Laureano-Ruiz AS. The role of transcriptional elements during neuronal inner ear development. [Internet] [Doctoral dissertation]. Rutgers University; 2021. [cited 2021 Apr 12].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/65455/.
Council of Science Editors:
Laureano-Ruiz AS. The role of transcriptional elements during neuronal inner ear development. [Doctoral Dissertation]. Rutgers University; 2021. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/65455/
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