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Дисертації з теми "Transcription; gene regulation; obesity"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Grossman, Sharon R. (Sharon Rachel). "Combinatorial gene regulation by transcription factors." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/128406.

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Анотація:

Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2019
Cataloged from PDF of thesis. "The Table of Contents does not accurately represent the page numbering"--Disclaimer page.
Includes bibliographical references.
Combinatorial gene regulation is encoded in enhancers and promoters in the form of binding sites for transcription factors (TFs), which collaboratively recruit the transcriptional machinery and drive gene expression. Using high-throughput and quantitative technologies developed by our lab and others, we studied TF binding sites in enhancers from numerous different cell types and regulatory systems, shedding light general principles of motif composition and organization in typical cellular regulatory elements. We find extensive synergy between TF binding sites, some with organizational constraints and some with flexible positioning. We demonstrate that different TFs bind at distinct positions within regulatory elements, suggesting a new type of architectural constraint in enhancers. Importantly, our analysis of both TF organization and cooperativity revealed distinctive patterns that separates TFs into potential functional classes. Together, our results suggest a structure of the regulatory code at the level of TF function and generate new hypotheses about regiospecific binding patterns and functions of TF classes within enhancers.
by Sharon R. Grossman.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology

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2

Deavall, Damian Gregory. "The physiological regulation of cholecystokinin gene transcription." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367183.

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3

Dunham, Lee. "Dynamic regulation of growth hormone gene transcription." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/dynamic-regulation-of-growth-hormone-gene-transcription(62354b9b-c755-43b6-a3f0-d108c32232c9).html.

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Many genes demonstrate highly dynamic pulsatile expression, with characteristic bursts of activity. Dynamic expression of the human prolactin (hPrl) gene in pituitary cells has previously been investigated identifying key temporal characteristics, influenced by the process of chromatin remodelling. Earlier work on the related pituitary human growth hormone (hGH) proximal promoter (-496/+1bp) indicated that it displayed similar dynamic behaviour. The human GH gene contains an extensive long-distance regulatory sequence, including a locus control region (-14/-32kbp) that has been shown to regulate chromatin remodelling and confer tissue-specificity of hGH expression. In this work I aimed to study dynamic regulation of the hGH gene promoter in detail. Initially I investigated the efficiency of several methods to express the luciferase gene in a 180kb hGH genomic fragment using bacterial artificial chromosome recombineering, to allow the investigation of single cell transcription dynamics. Although a functional recombinant BAC was not finalised during the course of the work, I carried out detailed time course studies using shorter hGH-reporter constructs. Using quantitative microscopy to study live single cells, I compared the dynamic characteristics of a 5kb hPrl promoter fragment with those of -840/+1bp and -3348/+1bp hGH-luciferase promoter-reporter constructs. Whilst previous hPrl analysis utilised a binary mathematical model assuming a simplified two-state (ON/OFF) process of gene transcription, I validated and applied a novel stochastic switch model (SSM), assuming instead that transcription rate can switch between any variable states at any time. Through doing so I observed an asymmetry in transcription rate switching, suggesting an all-or-nothing activation of a single UP-switch, with a greater number of rate decreasing DOWN-switches. The -3348/+1bp construct produced double the number of DOWN-switches, whilst the -840/+1bp construct produced 1.5 DOWN-switches in a 48h period. The cycling of transcriptional activity seen by the shorter construct was modified through the addition of forskolin, activating cAMP signalling. However, significant modification of the transcriptionally inactive refractory period seen with the -3348/+1bp construct (reduced from 3h to 1.9h) required histone modification through application of trichostatin A, a HDAC inhibitor. In conclusion, different promoter elements confer different transcriptional timing and dynamics. A subtler transcriptional modelling, such as used here in the SSM, reveals new insights into the phenomena of transcriptional switching, but the mechanisms involved remain to be determined.

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4

Pang, Ting-kai Ronald. "Transcriptional regulation of the human secretin receptor gene /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25059324.

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5

Mastrangelo, Peter. "Transcription regulation of the Saccharomyces cerevisiae actin gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ27461.pdf.

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6

Garnier, France. "Study of transcription regulation of the gene mdr1." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56986.

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In order to characterize cis-acting sequences and trans-acting factors important in regulating the expression of the mouse mdr1 gene, in vitro DNAsel footprinting experiments were carried out on a mdr1 promoter segment between positions $-$245 and +84, using nuclear protein extracts prepared from cell lines expressing different endogenous amounts of mdr1 mRNAs. Three footprinted sequences were detected on the non-coding strand of the $-$245 to +84 mdr1 promoter fragment (between -77 to -56, between -46 to -24, and between +5 and +15) with nuclear extracts from mdr1 expressing cells (CMT-93, LTA, and Y-1 cells). In addition, a specific footprinted sequence ($-$14 to +5) was detected on both strands only with nuclear extracts from the mdr1 non-expressing cell line (RAG cells) suggesting the presence and binding of a putative negative regulatory factor in these cells. However, replacement of this sequence in the mdr1 basal promoter ($-$93 to +84) by a heterologous, although similar positioned SV40 sequence did not restore promoter activity in RAG cells. The basal mdr1 promoter was further characterized in bidirectional deletion mutants, in order to identify cis-acting elements important for general transcriptional regulation. These studies further localized the mdr1 basal promoter between positions $-$74 and +84, and also suggested the presence of possible positive and negative cis-acting sequence elements modulating the activity of this basal promoter.

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7

Li, Yifan. "Gene regulation by WT1 and related transcription factors." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509772.

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8

Jahangiri, Leila. "Combinatorial gene regulation by T-domain transcription factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610328.

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9

Gay, Robert Daniel. "Neuronal gene regulation by POU family transcription factors." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267026.

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10

Tshuikina, Wiklander Marina. "Epigenetic Regulation of Gene Transcription in Hematopoietic Tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9206.

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11

Pang, Ting-kai Ronald, and 彭鼎佳. "Transcriptional regulation of the human secretin receptor gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243514.

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12

Dalton, Stephen. "Transcriptional regulation of histone gene expression /." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phd152.pdf.

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13

Lee, Tsz-on, and 李子安. "Transcriptional regulation of the human secretin gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30163389.

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14

Trowern, Angus Robert. "Regulation of the neurone-specific protein gene product (PGP) 9.5 gene." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262908.

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15

Nygård, Maria. "Regulation of gene transcription by the thyroid hormone receptors /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-756-1/.

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16

Holmqvist, Per-Henrik. "Transcription factor effects on chromatin organisation and gene regulation /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-453-8/.

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17

Miller, Christian. "Gene regulation during stress response transcription in Saccharomyces Cerevisiae." Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-155087.

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18

Hsu, Yu-Shen. "Regulation of transcription of a developmental gene in Dictyostelium." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268168.

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19

Inada, Akari. "The regulation of insulin gene transcription by CREM family." Kyoto University, 2001. http://hdl.handle.net/2433/150503.

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20

Ye, Chaoyang. "Transcription regulation of adeno-associated viruses." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4709.

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Анотація:

Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
"May 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

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21

Sasmono, R. Tedjo. "Transcriptional regulation of c-fms gene expression /." [St. Lucia, Qld.], 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17479.pdf.

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22

Wong, Kam Wai. "Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20WONGK.

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Анотація:

Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 95-108). Also available in electronic version. Access restricted to campus users.

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23

Kiełbasa, Szymon M. "Bioinformatics of eukaryotic gene regulation." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2006. http://dx.doi.org/10.18452/15562.

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Die Aufklärung der Mechanismen zur Kontrolle der Genexpression ist eines der wichtigsten Probleme der modernen Molekularbiologie. Detaillierte experimentelle Untersuchungen sind enorm aufwändig aufgrund der komplexen und kombinatorischen Wechselbeziehungen der beteiligten Moleküle. Infolgedessen sind bioinformatische Methoden unverzichtbar. Diese Dissertation stellt drei Methoden vor, die die Vorhersage der regulatorischen Elementen der Gentranskription verbessern. Der erste Ansatz findet Bindungsstellen, die von den Transkriptionsfaktoren erkannt werden. Dieser sucht statistisch überrepräsentierte kurze Motive in einer Menge von Promotersequenzen und wird erfolgreich auf das Genom der Bäckerhefe angewandt. Die Analyse der Genregulation in höheren Eukaryoten benötigt jedoch fortgeschrittenere Techniken. In verschiedenen Datenbanken liegen Hunderte von Profilen vor, die von den Transkriptionsfaktoren erkannt werden. Die Ähnlichkeit zwischen ihnen resultiert in mehrfachen Vorhersagen einer einzigen Bindestelle, was im nachhinein korrigiert werden muss. Es wird eine Methode vorgestellt, die eine Möglichkeit zur Reduktion der Anzahl von Profilen bietet, indem sie die Ähnlichkeiten zwischen ihnen identifiziert. Die komplexe Natur der Wechselbeziehung zwischen den Transkriptionsfaktoren macht jedoch die Vorhersage von Bindestellen schwierig. Auch mit einer Verringerung der zu suchenden Profile sind die Resultate der Vorhersagen noch immer stark fehlerbehafted. Die Zuhilfenahme der unabhängigen Informationsressourcen reduziert die Häufigkeit der Falschprognosen. Die dritte beschriebene Methode schlägt einen neuen Ansatz vor, die die Gen-Anotation mit der Regulierung von multiplen Transkriptionsfaktoren und den von ihnen erkannten Bindestellen assoziiert. Der Nutzen dieser Methode wird anhand von verschiedenen wohlbekannten Sätzen von Transkriptionsfaktoren demonstriert.
Understanding the mechanisms which control gene expression is one of the fundamental problems of molecular biology. Detailed experimental studies of regulation are laborious due to the complex and combinatorial nature of interactions among involved molecules. Therefore, computational techniques are used to suggest candidate mechanisms for further investigation. This thesis presents three methods improving the predictions of regulation of gene transcription. The first approach finds binding sites recognized by a transcription factor based on statistical over-representation of short motifs in a set of promoter sequences. A succesful application of this method to several gene families of yeast is shown. More advanced techniques are needed for the analysis of gene regulation in higher eukaryotes. Hundreds of profiles recognized by transcription factors are provided by libraries. Dependencies between them result in multiple predictions of the same binding sites which need later to be filtered out. The second method presented here offers a way to reduce the number of profiles by identifying similarities between them. Still, the complex nature of interaction between transcription factors makes reliable predictions of binding sites difficult. Exploiting independent sources of information reduces the false predictions rate. The third method proposes a novel approach associating gene annotations with regulation of multiple transcription factors and binding sites recognized by them. The utility of the method is demonstrated on several well-known sets of transcription factors. RNA interference provides a way of efficient down-regulation of gene expression. Difficulties in predicting efficient siRNA sequences motivated the development of a library containing siRNA sequences and related experimental details described in the literature. This library, presented in the last chapter, is publicly available at http://www.human-sirna-database.net

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24

Göndör, Anita. "Epigenetic Regulation of Higher Order Chromatin Conformations and Gene Transcription." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8296.

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Epigenetic states constitute heritable features of the chromatin to regulate when, where and how genes are expressed in the developing conceptus. A special case of epigenetic regulation, genomic imprinting, is defined as parent of origin-dependent monoallelic expression. The Igf2-H19 locus is considered as paradigm of genomic imprinting with a growth-promoting gene, Igf2, expressed paternally and a growth antagonist, H19 encoding a non-coding transcript, expressed only from the maternal allele. The monoallelic expression patterns are regulated by the epigenetic status at an imprinting control region (ICR) in the 5´-flank of the H19 gene. The chromatin insulator protein CTCF interacts with only the maternal H19 ICR allele to prevent downstream enhancers to communicate with the Igf2 promoters. Mutations of these CTCF binding sites lead to biallelic Igf2 expression, increased size of the conceptus and predisposition for cancer. Reasoning that these effects cannot be explained by the regulation of Igf2 expression alone, a technique was invented to examine long-range chromatin interactions without prior knowledge of the interacting partners. Applying the circular chromosomal conformation capture (4C) technique to mouse neonatal liver cells, it was observed that 114 unique sequences interacted with the H19 ICR. A majority of these interactors was in complex with only the maternal H19 ICR allele and depended on the presence of functional CTCF binding sites. The functional consequence of chromosomal networks was demonstrated by the observation that the maternal H19 ICR allele regulated the transcription of two genes on another chromosome. As the chromosomal networks underwent reprogramming during the maturation of embryonic stem cells, attention was turned to human cancer cells, displaying features common with mouse embryonic stem cells. Subsequently, chromatin folding at the human H19 ICR suggested that stable chromatin loops were organized by synergistic interactions within and between baits and interactors. The presence of these interactions was linked to DNA methylation patterns involving repeat elements. A "flower" model of chromatin networks was formulated to explain these observations. This thesis has unravealed a novel feature of the epigenome and its functions to regulate gene expression in trans. The identified roles for CTCF as an architectural factor in the organization of higher order chromatin conformations may be of importance in understanding development and disease ontogeny from novel perspectives.

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25

Cheng, Kwai Wa. "Transcription regulation of human gonadotropin-releasing hormone receptor gene expression." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61070.pdf.

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26

Kolodziej, Katarzyna Ewa. "Characterization of transcription factor complexes involved in globin gene regulation." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/11813.

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27

Dallosso, Anthony Richard. "Epigenetic regulation and transcription at the Wilms' tumour suppression gene." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288408.

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28

Richmond, Laura. "Development of engineered CRISPR transcription factors for programmable gene regulation." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30942/.

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29

Sykes, Michelle Christine. "Regulation of endothelial gene transcription by shear stress in a." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/24824.

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Анотація:

Thesis (Ph.D.)--Biomedical Engineering, Georgia Institute of Technology, 2008.
Committee Chair: Jo, Hanjoong; Committee Member: Griendling, Kathy; Committee Member: Harrison, David; Committee Member: Wang, May; Committee Member: Yoganathan, Ajit.

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30

Finch, Rosalynde J. "Regulation of interleukin-2 gene transcription in CD8 positive cells /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8352.

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31

VUILLAUMIER, BARROT SANDRINE. "Etude de la regulation transcriptionnelle du gene cftr." Paris 5, 1997. http://www.theses.fr/1997PA05N062.

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32

Smith, Stuart Barrie. "The role of transcription factor IUF1 in the regulation of insulin gene transcription by nutrients." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361786.

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This thesis gives insight into the way that transcription of the insulin gene is regulated by nutrients. This is achieved primarily by characterising a MAP kinase pathway which links glucose metabolism to the activation of a beta cell transcription factor IUF1. An understanding of the precise mechanisms by which nutrients control beta cell function may be invaluable for the development of artificial cell lines that can be used for gene replacement therapy. A study of the E2 element of the rat II promoter illustrated that at least three factors bound to the region. These were identified as IUF1 (complex D5), USF (complex D4) and an uncharacterised factor D3. IUF1 is a beta cell specific transcription factor that has been implicated previously in glucose responsive insulin gene transcription. IUF1 binds to the insulin promoter in response to high levels of extracellular glucose. USF has been shown to be involved in the carbohydrate responsive transcription of various hepatic genes. The recently characterised stress activated (Reactivating Kinase) MAP kinase pathway was clearly shown to be involved in mediating the link between glucose metabolism within the beta cell and the binding activity of IUF1. Phosphorylation of the factor serves to induce an alteration in protein structure, which converts the factor to an active form that shows a high affinity for its DNA binding site, thus activating transcription. The RK pathway may prove to be a crucial link between nutrient metabolism and the activity of other physiological processes.

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33

El-Kady, A. "A study on regulation of a transcription factor CTCF, by phosphorylation." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275324.

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34

Tsai, Pei-Fang. "TAF1 regulation of gene expression genome-wide localization and transcription profiling /." Diss., [Riverside, Calif.] : University of California, Riverside, 2010. http://proquest.umi.com/pqdweb?index=0&did=2019822761&SrchMode=2&sid=1&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1273863805&clientId=48051.

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Анотація:

Thesis (Ph. D.)--University of California, Riverside, 2010.
Includes abstract. Available via ProQuest Digital Dissertations. Title from first page of PDF file (viewed April 24, 2010). Includes bibliographical references. Also issued in print.

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35

Rada-Iglesias, Alvaro. "From Single Gene to Whole Genome Studies of Human Transcription Regulation." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7463.

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36

Subramaniam, Nanthakumar. "Transcription factors involved in negative and positive gene regulation by glucocorticoids /." Stockholm, 1999. http://diss.kib.ki.se/1999/19990115subr/.

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37

Huang, Charlie Chia Wei. "Regulation of Cat-1 gene transcription during physiological and pathological conditions." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270242874.

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38

Donovan, Benjamin Thomas. "Nucleosome Regulation of Transcription Factor Binding Kinetics: Implications for Gene Expression." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1574774626880568.

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39

Chang, Miao. "Cell type specific regulation of human placenta growth factor gene transcription /." Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1597612421&sid=3&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Анотація:

Thesis (Ph.D.)--Southern Illinois University Carbondale, 2008.
"Department of Molecular Biology, Microbiology and Biochemisty." Includes bibliographical references (p. 123-150). Also available online.

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40

Khoyratty, Tariq. "Interferon regulatory factor 5 : a systematic study of macrophage gene regulation." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:b820f612-ceb7-4e2c-af26-52999e368c41.

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Macrophages are multifaceted innate immune cells, able to adapt their phenotype to respond to a myriad of conditions, engaging in tissue-specific functions and mediating either inflammatory or anti-inflammatory responses depending on the encountered stimuli. They conduct key roles in the orchestration of immune responses; from pathogen recognition through sterilising inflammation to resolution and repair. The Udalova laboratory has previously demonstrated that IRF5 promotes a pro- inflammatory macrophage phenotype, leading to the secretion of TNF, IL-12, and IL-23, enhancing Th1/Th17-mediated immune responses, and described the cooperation between IRF5 and the transcription factor RelA, which mediate the production of pro-inflammatory genes. The aim of this thesis is to further characterise the activity of IRF5 in macrophage inflammatory responses. I demonstrate that IRF5 not only regulates the transcription of cytokines and chemokines in response to bacterial stimuli, but also anti-microbial peptides, whilst simultaneously down-regulating homeostatic and resolving macrophage functions. My data also suggests that IRF5 plays a role in enforcing monocyte to macrophage differentiation by up-regulating the transcription of key macrophages markers and repressing dendritic cell identity genes. To further characterise the mechanisms of the inflammatory response mounted by macrophages I used an unbiased approach; combining twenty-three transcription factor ChIP-seq data sets with chromatin accessibility information from ATAC-seq, uncovering RUNX1 as a novel partner of IRF5 that binds co-operatively to clusters of enhancers, which control the transcription of pro-inflammatory genes in a signal-dependent manner. This is the first study demonstrating a critical role for RUNX1 in activity of inflammatory macrophages.

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41

Xia, Ninuo. "Non-coding RNA's role in epigenetic gene regulation." Diss., UC access only, 2009. http://proquest.umi.com/pqdweb?index=109&did=1871884811&SrchMode=1&sid=1&Fmt=7&retrieveGroup=0&VType=PQD&VInst=PROD&RQT=309&VName=PQD&TS=1270486124&clientId=48051.

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Thesis (Ph. D.)--University of California, Riverside, 2009.
Includes abstract. Includes bibliographical references (leaves 105-122). Issued in print and online. Available via ProQuest Digital Dissertations.

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42

Panjaworayan, Nattanan, and n/a. "Post-transcriptional regulation of gene expression in Hepatitis B virus." University of Otago. Department of Biochemistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20071218.143835.

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Hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma and liver cirrhosis worldwide. HBV vaccination can prevent new infections, but effective antiviral drugs are not available for a large number of HBV infected patients. To develop novel antiviral drugs, a better understanding of the regulation of HBV gene expression is vital. One important aspect is to understand how HBV hijacks the cellular machinery to export unspliced RNAs from the nucleus of a cell to the site of incorporation into new HBV particles. The HBV post-transcriptional regulatory element (HBV PRE) is a cis acting RNA element found in all HBV transcripts. It has been reported to play an important role in the nuclear export of HBV mRNAs. Moreover, it has the ability to enhance expression of intronless as well as unspliced transcripts. Despite concerted investigations, the functional core element of HBV PRE remains unknown and the exact mechanism of how HBV PRE mediates nuclear export is unclear. This project first produced a complete HBV genome with comprehensive annotation of both coding regions and regulatory signals, which was then used for comparative genomic analysis. The functional elements of the HBV PRE were first subjected to analysis in silico. The HBV PRE is highly conserved among HBVs. Based on this sequence conservation and prediction of conserved RNA secondary structure, potentially functional HBV PRE elements including the previously reported elements (HBV SLα and HBV SLβ) were identified. Experimental deletion analysis of the HBV PRE sequence showed that the effect of each of these elements on the intronless reporter gene�s expression was similar to that of the entire full length HBV PRE. Thus, the results suggested that overall HBV PRE function was not due to additive effects from the individual elements. Surprisingly, a specific sub-section of HBV PRE decreased the level of reporter gene expression. This sub-section has not been identified previously, thus it is a novel HBV PRE inhibitory element. Further analyses using specific reporter assays revealed that the HBV PRE enhanced expression of an unspliced reporter gene whereas the RNA nuclear export elements of retroviruses, CTE (in MPMV) and RRE (in HIV-1) were not able to. Therefore, these results indicate that HBV PRE is involved in inhibition of splicing and it utilizes a different mechanism from CTE and RRE. Interestingly, HBV PRE was observed to be unable to enhance the expression of an intronless luciferase gene. Therefore, HBV PRE is not able to enhance cytoplasmic expression of all intronless transcripts. This project also addressed the idea that the RNA-binding protein, polypyrimidine tract binding protein (PTB) is a positive trans-acting factor for HBV PRE function. Transient expression of exogenous PTB in cultured cells showed no specific effect on constructs containing HBV PRE. Moreover, reduction of endogenous PTB by RNAi did not affect HBV PRE function. Therefore, the results presented in this project do not support the hypothesis that PTB plays a role in HBV PRE function. Given that HBV PRE is highly conserved and present in all HBV transcripts, it makes a good target site for novel molecular therapeutic treatments such as siRNA. To identify potential siRNA target sites within HBV PRE, an RNAi study using a plasmid expressing shRNA against HBV PRE was done. The results from the RNAi study revealed that the expression of a reporter gene could be significantly reduced by siRNA targeted to the HBV PRE. Overall, this project produced a highly annotated HBV genome that can be used as the reference sequence for comparative genomic analysis. Moreover, this work identified novel regulatory elements within HBV PRE that are likely to play an important role in HBV gene expression. Furthermore, the study also identified an excellent siRNA target site within HBV PRE that may inhibit HBV gene expression.

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43

Jawdekar, Gauri W. "Transcriptional regulation of the human small nuclear RNA gene family." Diss., Connect to online resource - MSU authorized users, 2006.

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Thesis (Ph. D.)--Michigan State University. Dept. of Microbiology and Molecular Genetics, 2006.
Title from PDF t.p. (viewed on June 19, 2009) Includes bibliographical references. Also issued in print.

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44

Hock, Thomas D. "Regulation of the human heme oxygenase-1 gene." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/hock.pdf.

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45

Eisen, Timothy George Quentin. "Regulation of cell type-specific gene expression in melanocytes and melanoma." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336364.

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46

Grzeskowiak, Rafal. "Involvement of the paired-domain transcription factor Pax6 in the regulation of glucagon gene transcription by insulin." Doctoral thesis, [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961362200.

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47

Ho, Siu-hong. "Characterization of the transcriptional regulation of C. elegans mab-21 gene and its genetic partner, a sin3-like gene /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20HO.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 175-187). Also available in electronic version. Access restricted to campus users.

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48

Almeida, Diego Melo. "Regulation of the OsNHX1 Gene Expression: Identification and Characterization of Novel Transcription Factors." Doctoral thesis, Instituto de Tecnologia Química e Biológica António Xavier. Universidade Nova de Lisboa, 2016. http://hdl.handle.net/10362/51890.

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For half of the world´s population, rice is life. This cereal crop is considered an important staple food worldwide, and more than three billion people count on it for 50-80% of their daily calorie intake. Soil salinity is a major environmental constraint to crop production, resulting in considerable yield losses around the globe every year. According to the Food and Agriculture Organization (FAO), in 2008 over 6% of world's total land and over 20% of irrigated land were affected by high levels of salt. Irrigated land is only 15% of cultivated land, but it produces one third of the world’s food, raising awareness about salinity as a serious problem for crop productivity. Rice like as most crops is very sensitive to salt, showing salt stress symptoms and reduced yield at relatively low soil salinity levels (≈ 40 mM NaCl). Among the agronomically important cereals, rice shows the highest sensitivity to salt. However, some degree of genotype tolerance for salt stress is available in rice germplasm. To cope with salt stress conditions, plants evolved several and diverse response mechanisms. One of these mechanisms is tissue tolerance, in which high salt concentration is found in leaves but is compartmentalized, especially in the vacuole, reducing the deleterious effect of Na+ in the cytosol and driving water uptake to cells. Cation/H+ antiporters mediate the transport of Na+ into the vacuole.(...)
info:eu-repo/semantics/publishedVersion

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49

West, Adam Geoffrey. "Molecular interactions of the MADS-box transcription factors." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362415.

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50

Dunn, Stephanie May. "Transcription factors involved in regulation of immune and haemopoietic cytokine gene expression." Adelaide Thesis (Ph.D.) -- University of Adelaide, Department of Microbiology and Immunology, 1993. http://hdl.handle.net/2440/21642.

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Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1993

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