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Dissertations / Theses on the topic 'Transcription by bacterial RNA polymerase'

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Published: 4 June 2021
Last updated: 4 February 2022

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1

Ferguson, Anna Louise. "Interactions of bacterial sigma subunits with core RNA polymerase." Thesis, University of York, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341839.

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2

Southern, Emma. "The role of #sigma#'54 region II in transcription initiation." Thesis, University of East Anglia, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302057.

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3

Furman, Ran. "DksA Beyond the Stringent Response: Investigating the Functions of a Diverse Bacterial Transcription Factor." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1367584519.

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4

Tupin, Audrey. "Inhibiteurs de la transcription bactérienne : étude du mécanisme d'action de la lipiarmycine et dépendance au facteur de transcription σ." Thesis, Montpellier 1, 2010. http://www.theses.fr/2010MON13512/document.

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Le nombre croissant de bactéries résistantes aux antibiotiques et le problème des cellules persistantes rend urgent le développement de nouveaux antibiotiques et la compréhension de leur mécanisme d'action. L'ARN polymérase est l'enzyme centrale de la transcription et est une cible intéressante pour les antibiotiques. Dans cette étude, nous nous sommes particulièrement intéressés à un inhibiteur de l'ARN polymérase : la lipiarmycine. Il s'agit d'un inhibiteur de la transcription macrocyclique qui inhibe les bactéries à Gram + et qui est en essai clinique de phase III pour le traitement des infections liées à Clostridium difficile. L'objectif de ce travail a été de déterminer le mécanisme d'action de la lipiarmycine ainsi que le mécanisme de résistance à la molécule. Pour cela, nous avons dans un premier temps précisé et modélisé son site de liaison sur l'ARN polymérase. Puis, dans un deuxième temps, nous avons utilisé des approches génétiques et biochimiques afin de déterminer son mécanisme et l'effet de certaines mutations sur la transcription. Ces travaux ont mis à jour un nouveau mécanisme d'inhibition de la transcription
The growing number of antibiotic-resistant bacteria added to the problem caused by persistent cells stress the need for developing new antibiotics and for understanding their mechanism of action. RNA polymerase is the main enzyme of the transcription process and is an interesting target for antibiotics. In this study we focus on a particular inhibitor of RNA polymerase : lipiarmycin. It is a macrocyclic inhibitor of transcription inhibiting Gram + bacteria that is developed in phase III clinical trials for treatment of Clostridium difficile infections. The objective of this work was to determine the mechanism of action of lipiarmycin and the mechanism confering resistance against the molecule. We first define more precisely its binding site on RNA polymerase and then used genetic and biochemical approaches to determine its mechanism of action and the effect of some specific mutations on transcription. Our experiments reveal a new mechanism of t ranscription inhibitor action
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5

Chakraborty, Atanu. "Mechanism Of mom Gene Transactivation By Transcription Factor C Of Phage MU." Thesis, Indian Institute of Science, 2006. http://hdl.handle.net/2005/275.

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Regulation of transcription initiation is the major determining event employed by the cell to control gene expression and subsequent cellular processes. The weak promoters, with low basal transcription activities, are activated by activators. Bacteriophage Mu mom gene, which encodes a unique DNA modification function, is detrimental to cell when expressed early or in large quantities. Mu has designed a complex, well-controlled and orchestrated regulatory network for mom expression to ensure its synthesis only in late lytic cycle. The phage encoded transcription activator protein C activates the gene by promoter unwinding of the DNA and thereby recruiting of RNAP to the promoter. C protein functions as a dimer for DNA binding and transcription activation. Mutagenesis and chemical crosslinking studies revealed that the leucine zipper motif, and not the coiled coil motif in the N terminal region, is responsible for C dimerization. The DNA binding domain of C is a HTH domain which is preceded by the leucine zipper motif. The C protein is one of the few examples in the bacterial proteins containing both leucine zipper and HTH domain. Most of the transcription activators either influence initial binding of RNAP or conversion of closed to open complex formation. Very few activators act at subsequent steps of promoter-polymerase interaction. Earlier studies showed high level of transcription from a mutant mom promoter, tin7. Addition of C further increased transcription from Ptin7 indicating that C may have a role beyond polymerase recruitment. Each steps of transcription initiation have been dissected using the Ptin7 and a positive control (pc) mutant of C, R105D. The results revealed multi-step transcription activation mechanism for C protein at Pmom. C recruits RNAP at Pmom and subsequently increases the productive RNAP-promoter complex and enhances promoter clearance. To further understand the C mediated transactivation mechanism, interaction between C and RNAP was assessed. C interacts with holo and core RNAP only in presence of DNA. Positive control mutants of C, F95A and R015D, were found to be compromised in RNAP interactions. These mutants were efficient in RNAP recruitment to Pmom but do not enhance promoter clearance. Trypsin cleavage protection experiment indicated that probably C protein interacts with b¢ subunit of RNAP. Interaction between C and RNAP appears to enhance the formation of productive RNAP-promoter complex leading to promoter clearance. The connection between activator-polymerase interaction and transcription activation is well documented where the recruitment of RNAP is influenced. In case of activators acting at post recruitment steps of initiation, the role of polymerase contact is poorly understood. Our study shows that activator-polymerase interaction can lead to increased promoter clearance at Pmom by overcoming abortive initiation.
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6

Duval-Valentin, Guy. "Reconnaissance proteines-acides nucleiques : etudes structurales et dynamiques de l'interaction de l'arn-polymerase d'e. coli sur deux promoteurs aux comportements heterologues." Paris 6, 1987. http://www.theses.fr/1987PA066354.

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7

Fernández, Coll Llorenç. "Secondary channel of the RNA polymerase, a target for transcriptional regulation in bacteria." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/298719.

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Gene expression begins by an enzymatic complex known as RNA polymerase (RNApol). The basic unit (core) of RNApol in bacteria is formed by 5 protein subunits (α2ββ’ω). The three-dimensional structure of the RNApol defines two spaces that play a relevant role during transcription, defined as primary and secondary channel. The holoenzyme needs the binding of a σ subunit to recognise promoter sequences and initiate the transcription process. Transcription is a dynamic process controlled at different steps. Genetic regulation during transcription initiation has been highly studied, and several mechanisms of regulation exist. However, the aim of this project is to study some aspects of the regulation during transcription elongation. It has been described that the alamone ppGpp, as well as several proteins, such as GreA, GreB or DksA, enter within the secondary channel and interact directly with the catalytic centre of the RNApol. The swap between the different factors that bind to the secondary channel of the RNApol may cause changes in the expression pattern. It has been postulated that DksA and ppGpp act as cofactors, however, a previous study performed in our research group, indicated that the phenotype of ppGpp and DksA deficiencies were not always identical, letting us suggest that the occupancy degree of the secondary channel of the RNApol may have significant impact in the expression pattern in E. coli. The data obtained clearly indicate that upregulation of some genes, such as fliC, that occurs in absence of DksA, was the result of the vacancy of the secondary channel generated in a dksA strain rather than being the result of DksA having a direct repressor effect. We suggested that in the absence of DksA, the interactions of other proteins, such as GreA, are promoted and responsible of the upregulation observed. In this project, functional, structural and phylogenetical studies of the protein GreA were performed to determine which amino acids are important for i) the functionality of GreA, ii) the ability to bind to the secondary channel of the RNApol or iii) the capacity to compete with other factors, such as DksA. We have determined that greA overexpression produces a negative effect of the bacterial growth. Moreover, this negative effect is enhanced in absence of DksA, highlighting the hypothesis of a competition between factors that bind into the secondary channel. The effect of this competition between GreA and DksA was also determined studying the expression of the fliC gene. Our data showed that both, GreA and DksAare required for fliC expression but act at different levels in the regulatory cascade of flagella expression regulation. GreA may control fliC expression during transcription elongation whereas DksA may act during transcription initiation. Changes in the amount of GreA, could affect the competition between factors that bind to the secondary channel of the RNApol. Therefore, we have determined the expression pattern of greA. Transcriptional studies showed a crosstalk between the different factors that bind into the secondary channel of the RNApol exists. Finally, transcriptomic studies were performed to determine the effect of ppGpp and DksA on the expression pattern of Salmonella enterica serovar Typhimurium. The results obtained indicate : i) the effect of the possible competence between the factors that interact into the secondary channel of the RNApol and ii) the effect of ppGpp and DksA on the expression of several virulence factors as well as different mobile elements present in Salmonella.
El control de l’expressió gènica en bacteris recau principalment sobre un complex enzimàtic anomenat ARN polimerasa (ARNpol). A procariotes, la seva unitat bàsica (core) està formada per 5 subunitats proteiques (a2bb’w). S’han determinat dos canals entre les diferents subunitats de l’ARNpol: el canal primari, on es desenvolupa la transcripció, i el canal secundari, que comunica el medi exterior amb el centre catalític de l’ARNpol. Tot i així, aquest holoenzim necessita la unió d’una subunitat σ per ser capaç de reconèixer una seqüència promotora i iniciar la transcripció. S’han descrit diferents factors, tant proteics com no proteics, que poden interaccionar amb el canal secundari de l’ARNpol i causar alteracions a l’expressió gènica. En aquesta tesi ens hem centrat en la possible competència entre els diferents factors que poden interaccionar amb el canal secundari de l’ARNpol. Estudis anterior duts a terme en el nostre grup d’investigació, ens van permetre postular una possible competència entre els diferents factors que interaccionen amb el canal secundari de l’ARNpol, més concretament entre les proteïnes GreA i DksA. Aquesta competència provocaria alteracions en el patró d’expressió gènica d’Escherichia coli. En aquest treball s’han dut a terme estudis funcionals, estructurals i filogenètics de la proteïna GreA que ens han permès determinar quins aminoàcids, i com a conseqüència quins dominis, podrien ser importants per la funcionalitat de la proteïna, la seva capacitat d’unir-se a l’ARNpol i la seva capacitat de competir amb altres factors. A més, hem estudiat quin efecte té la competència entre els diferents factors que interaccionen amb el canal secundari sobre l’expressió d’un gen diana. Canvis en els nivells de la proteïna GreA, poden afectar la competència pel canal secundari de l’ARNpol Per això hem determinat el patró d’expressió del gen greA, així com l’existència d’una regulació creuada entre les diferents proteïnes que interaccionen amb el canal secundari. Finalment, hem dut a terme un estudi transcriptòmic en Salmonella enterica serovar Typhimurium, amb l’objectiu de determinar quin és l’efecte d’aquesta competència en l’expressió de factors de virulència.
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8

Neugebauer, Karla M., Inna Grishina, Anita S. Bledau, and Imke Listerman. "Extragenic Accumulation of RNA Polymerase II Enhances Transcription by RNA Polymerase III." PLOS, 2007. https://tud.qucosa.de/id/qucosa%3A27951.

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Recent genomic data indicate that RNA polymerase II (Pol II) function extends beyond conventional transcription of primarily protein-coding genes. Among the five snRNAs required for pre-mRNA splicing, only the U6 snRNA is synthesized by RNA polymerase III (Pol III). Here we address the question of how Pol II coordinates the expression of spliceosome components, including U6. We used chromatin immunoprecipitation (ChIP) and high-resolution mapping by PCR to localize both Pol II and Pol III to snRNA gene regions. We report the surprising finding that Pol II is highly concentrated ∼300 bp upstream of all five active human U6 genes in vivo. The U6 snRNA, an essential component of the spliceosome, is synthesized by Pol III, whereas all other spliceosomal snRNAs are Pol II transcripts. Accordingly, U6 transcripts were terminated in a Pol III-specific manner, and Pol III localized to the transcribed gene regions. However, synthesis of both U6 and U2 snRNAs was α-amanitin-sensitive, indicating a requirement for Pol II activity in the expression of both snRNAs. Moreover, both Pol II and histone tail acetylation marks were lost from U6 promoters upon α-amanitin treatment. The results indicate that Pol II is concentrated at specific genomic regions from which it can regulate Pol III activity by a general mechanism. Consequently, Pol II coordinates expression of all RNA and protein components of the spliceosome.
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9

Neugebauer, Karla M., Inna Grishina, Anita S. Bledau, and Imke Listerman. "Extragenic Accumulation of RNA Polymerase II Enhances Transcription by RNA Polymerase III." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-184076.

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Recent genomic data indicate that RNA polymerase II (Pol II) function extends beyond conventional transcription of primarily protein-coding genes. Among the five snRNAs required for pre-mRNA splicing, only the U6 snRNA is synthesized by RNA polymerase III (Pol III). Here we address the question of how Pol II coordinates the expression of spliceosome components, including U6. We used chromatin immunoprecipitation (ChIP) and high-resolution mapping by PCR to localize both Pol II and Pol III to snRNA gene regions. We report the surprising finding that Pol II is highly concentrated ∼300 bp upstream of all five active human U6 genes in vivo. The U6 snRNA, an essential component of the spliceosome, is synthesized by Pol III, whereas all other spliceosomal snRNAs are Pol II transcripts. Accordingly, U6 transcripts were terminated in a Pol III-specific manner, and Pol III localized to the transcribed gene regions. However, synthesis of both U6 and U2 snRNAs was α-amanitin-sensitive, indicating a requirement for Pol II activity in the expression of both snRNAs. Moreover, both Pol II and histone tail acetylation marks were lost from U6 promoters upon α-amanitin treatment. The results indicate that Pol II is concentrated at specific genomic regions from which it can regulate Pol III activity by a general mechanism. Consequently, Pol II coordinates expression of all RNA and protein components of the spliceosome.
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10

White, Eleanor. "Transcription termination by RNA polymerase II." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558432.

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RNA Polymerase II (Pol I1) is responsible for the transcription of all protein-encoding genes. Pol II termination is dependent on RNA processing signals (both terminal intron splice sites, and cleavage and polyadenylation signals) as well as specific terminator elements located downstream of the poly(A) site. Detailed analysis of the human ~- globin gene terminator has shown that it contains a sequence-specific region that promotes rapid Co-Transcriptional Cleavage (CoTC) of the nascent transcript - an essential but not well understood step in the human ~-globin gene termination process. In the first part of this thesis, the role of sequences within this CoTC-mediated terminator element in the termination process is investigated. Analysis of mutant terminator sequences indicate that homopolymer A tracts are important for Pol II termination. The second part of this study focuses on identifying the activity responsible for CoTC, by using the yeast S. pombe as a tool for genetic analysis. The results indicate that the human ~-globin gene terminator is inefficient in S. pombe, suggesting that a mammalian specific factor(s) are required. In the final part of this study, I describe an investigation into the possibility that the exosome subunit Dis3 or the RNase III enzyme Dicer are involved in CoTC mediated transcription termination. While Dis3 is not involved in the CoTC process my results on Dicer may imply a significant role. Lastly, I present a preliminary investigation into the effect of pre-mRNA processing and the carboxyl terminal domain (CTD) of Po 1 II on CoTC activity.
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11

Lee, Sally. "Architecture of RNA polymerase II and RNA polymerase III pre-initiation transcription complexes /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/9213.

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12

Niedbala, Angela Rochelle. "Kinetic studies of transcription initiation by wild type T7 RNA polymerase, his-tagged wild type T7 RNA polymerase and GP1-Lys222 T7 RNA polymerase." Thesis, Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/27288.

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13

Emili, Andrew. "Activation of RNA polymerase II mediated transcription." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0004/NQ27918.pdf.

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14

Kollakowski, Tanja Anna. "Regulation of Transcription by RNA Polymerase II." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491272.

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RNA Polymerase II (Pol II) transcribes mRNA genes, snRNA genes and histone genes. Whereas mRNA genes often contain introns, snRNA genes are intron-Iess. mRNA genes have a polyadenylation signal and snRNA genes contain a gene-specific 3' end processing signal, the 3' box. The length of a U2 snRNA transcription unit is approximately 1 kB, whereas that ofa mRNA gene is often thousands ofbase pairs long. A snRNA promoter is required for efficient 3' box processing. I have confIrmed these results but my data also show that a snRNA promoter can direct synthesis of poly (A) tails efficiently. It has been demonstrated that 3' box processing requires the conserved carboxyl tenninal domain (CTD) of pol II. It has been shown that the phosphorylation of the CTD on serine 2 by P-TEFb is essential for efficient 3' box processing. P-TEFb is also an elongation factor in the transcription ofmRNA genes. Two elements that have been reported to recmit P-TEFb were introduced into the U2 and the H2b gene: the HIV-I TARffat complex and an intron. I have shown that the HIV-I TARffat complex introduced into a U2 construct interferes with 3' box processing and . increases the size of the transcription unit. However, the TARfTat complex is compatible with H2b 3' end processing. These effects suggest a possible change of P-TEFb function through HIV-I TARfTat from snRNA 3' box processing to mRNA elongation factor. A synthetic PY7 intron was introduced into both genes. It is spliced efficiently. No disabling of the promoter-specific 3' end is detectable in either gene. The site of transcription termination is unaffected by the PY7 intron. It was concluded that the characteristic lack of introns in histone and snRNA genes is not a requirement for efficient, gene-specific 3' end processing. Substitution of the CMV promoter for a snRNA promoter has a negative effect on 3' box processing as well as an increase in the size of the transcription unit, emphasizing the importance of the promoter in defining the method of 3' end processing and the size of the transcription unit.
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15

Engel, Christoph. "RNA polymerase I structure and transcription regulation." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-173904.

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16

Ranish, Jeffrey A. "Mechanisms of transcription by RNA Polymerase II /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/5057.

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17

Sutcliffe, Josephine E. "The regulation of RNA polymerase I and RNA polymerase III transcription by the pocket proteins." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327577.

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18

Athineos, Dimitris. "Regulation of RNA polymerase III transcription during differentiation." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418905.

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19

Hengartner, Christoph J. (Christopher Johannes) 1968. "Regulation of yeast RNA polymerase II holoenzyme transcription." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85247.

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20

Burger, Kaspar. "CDK9 links RNA polymerase II transcription to processing of ribosomal RNA." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-167037.

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21

Grierson, Patrick Michael. "The BLM helicase facilitates RNA polymerase I-mediated ribosomal RNA transcription." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337865492.

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22

Shah, Sheila Marie Alojipan. "Studies on RNA polymerase III transcription : Structural organization of transcription factor IIIb /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3025949.

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23

Ringel, Eva Rieke. "Molecular basis of RNA polymerase III transcription repression by Maf1 & Structure of human mitochondrial RNA polymerase." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-134070.

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24

Stock, Julie Katherine. "Investigating RNA Polymerase II Phosphorylation in Transcription and Epigenetics." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498975.

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25

Goodfellow, Sarah Jayne. "Regulation of RNA polymerase III transcription during cardiomyocyte hypertrophy." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415260.

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26

Colbert, Trenton. "Characterization of BRF1, an RNA polymerase III transcription factor /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6320.

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27

Nayak, Dhananjaya. "Conformational mechanisms in T7 RNA polymerase transcription a dissertation /." San Antonio : UTHSC, 2008. http://learningobjects.library.uthscsa.edu/cdm4/item_viewer.php?CISOROOT=/theses&CISOPTR=44&CISOBOX=1&REC=11.

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28

Khoo, Bernard Chong Eu. "Mechanisms and regulation of RNA polymerase III transcription initiation." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627289.

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29

Bailey, Paul Austyn. "Inhibition of T7 RNA polymerase by T7 lysozyme." Diss., Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/30418.

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30

Chisholm, Robert David. "Mutations in RNA polymerase II that affect poly (a)-dependent termination /." view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1188876151&sid=1&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2006.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 80-86). Also available for download via the World Wide Web; free to University of Oregon users.
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31

Sheppard, Carol Maria. "Characterisation of bacteriophage-encoded inhibitors of the bacterial RNA polymerase." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/10960.

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RNA polymerase (RNAP) is an essential enzyme which catalyses transcription; a highly regulated process. Bacteriophage are viruses which infect bacteria and as a result have evolved a diverse range of mechanisms to regulate the bacterial RNAP to serve the needs of the virus. T7 Gp2 and Xp10 P7 are two bacteriophage-encoded transcription factors that inhibit the activity of the bacterial RNAP. The aim of this study is to investigate the molecular mechanisms of action of Gp2 and P7. Fluorescence anisotropy experiments proved Gp2 to bind to RNAP, independently of the σ- factor, with a 1:1 stoichiometry and a low nanomolar affinity. In vitro transcription assays demonstrated that a negatively charged strip in Gp2 is the major determinant for its inhibitory activity. Furthermore, it was shown that efficient Gp2-mediated inhibition of RNAP also depends upon the highly negatively charged and flexible σ70 specific domain, R1.1. Gp2 and R1.1 both bind in the downstream-DNA binding channel and exert long-range antagonistic effects on RNAP-promoter DNA interactions around the transcription start site. A systematic mutagenesis screen was used to identify residues in P7 necessary for binding to the RNAP; results were interpreted in the context of a newly resolved NMR structure of P7. Electrophoretic mobility shift assays revealed that P7 ‘traps’ a RNAP-promoter DNA complex en route to the transcriptionally-competent complex. Preliminary results from a fluorescence based RNAP-DNA interaction assay suggest that P7 may target RNAP interactions with the -35 promoter element and the ‘discriminator region’. This study has contributed to our understanding of how non-bacterial transcriptional factors can influence bacterial gene expression by modulating RNAP activity. This study has also uncovered vulnerabilities in RNAP, which have the potential to be exploited therapeutically. To this end, these structure-function studies of Gp2 and P7 have provided the basis for the rational design of novel anti-bacterial compounds.
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32

Kantidakis, Theodoros. "In vivo studies of repressors of RNA polymerase III transcription." Thesis, Thesis restricted. Connect to e-thesis to view abstract, 2008. http://theses.gla.ac.uk/161/.

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Thesis (Ph.D.) - University of Glasgow, 2008.
Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.
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33

Moreland, Rodney J. "Molecular interactions in RNA polymerase II and III transcription systems /." Full-text version available from OU Domain via ProQuest Digital Dissertations, 1998.

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34

Xiong, Yalin. "Downstream NTP effects on human RNA polymerase II transcription elongation." Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph.D.)--Michigan State University. Dept. of Biochemistry and Molecular Biology, 2008.
Title from PDF t.p. (viewed on Apr. 2, 2009) Includes bibliographical references. Also issued in print.
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35

Gopalan, Sneha. "Regulation of transcription by RNA polymerase II in S. pombe." Thesis, Open University, 2018. http://oro.open.ac.uk/53696/.

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An understanding of the mechanisms underlying the various stages of transcription is crucial to find solutions to the problems caused by mis-expression of genes that may give rise to a host of human diseases. My thesis research focusses on an analysis of the RNA Polymerase II elongation factor Ell1/Eaf1 in S. pombe. Eleven-nineteen lysine-rich in leukemia (ELL) is encoded by a gene involved in translocations with MLL in leukemia and forms a tight complex with ELL-associated factors (EAF). ELL/EAF is an RNA polymerase II elongation factor that in metazoa can assemble into a larger assembly that also includes P-TEFb and other proteins encoded by genes involved in MLL translocations. This larger assembly, sometimes called SEC, binds to a specific "docking site" in the metazoan Mediator complex. Distantly related ELL- and EAF-like genes were identified in S. pombe that encode Ell1/Eaf1 and can stimulate Pol II elongation in vitro. My thesis addresses two distinct projects, with overlapping motivations: First, to see whether S. pombe might provide a good model for functional studies of the Mediator and ELL/EAF interaction, I carried out a thorough proteomic analysis of S. pombe Mediator and defined several new subunits. My results were recently published as part of a collaborative structural analysis of S. pombe Mediator. Second, I used a combination of biochemical, genetic, and genomic approaches to characterize Ell1/Eaf1 function in fission yeast. Using mass spectrometry, I identified an uncharacterized sequence orphan, SPAC6G9.15c, that associates with both Ell1 and Eaf1 to form a ternary complex that, based on ChIP-seq localizes at genes with high RNA Pol II occupancy. I also performed an SGA screen for genes that genetically interact with ell1, eaf1, and SPAC6G9.15c and identified a set of overlapping genes that interact with all three, as well as others that interact only with ell1.
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36

Abdelkareem, Moamen. "Structural basis of transcription : RNA polymerase backtracking and its reactivation." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ062.

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Ma thèse se focalise sur la compréhension d’un phénomène de transcription, appelé backtracking, qui inactive la RNAP et arrête la transcription. La réactivation des complexes RNAP arrêtés et la reprise de la transcription nécessitent un facteur protéique appelé GreB. L’objectif du projet était d’obtenir des informations structurelles sur: i) la façon dont le retour en arrière inactive la RNAP dans E. coli; et ii) comment GreB sauve la RNAP en marche arrière pour continuer la transcription. À l'aide de SP cryo-EM, j’ai capturé quatre instantanés de RNAP dans différents états. Mes résultats montrent que l'ARN n'est plus aligné avec le site actif. De plus, suite à un retour en arrière, la RNAP adopte de nouvelles modifications de conformation permettant la liaison de GreB. En conséquence, le NTD de GreB entre en contact le site actif de la RNAP et donne des résidus acides qui augmentent l'affinité pour un ion magnésium, ce qui est nécessaire pour la catalyse du clivage de l'ARN mal aligné. Ces quatre reconstructions donnent un aperçu du mécanisme catalytique et de la dynamique du clivage et de l'extension de l'ARN
[...]My Ph.D. was focused on the understanding of a transcriptional phenomenon, termed backtracking, which inactivates RNAP and halts transcription. Reactivation of halted RNAP complexes and transcription resumption, requires a protein factor called GreB. The objective of the project was to gain structural information on: i) how backtracking inactivates RNAP inE. coli; and ii) how GreB rescues backtracked RNAP to continue transcription. Using SP cryo- EM, I captured four snapshots of RNAP at different states covering the backtracking and reactivation cycle. My results show that the RNA is no longer aligned with the active center, explaining the transcription halt. Furthermore, as a result of backtracking, RNAP adopts new conformational changes allowing GreB binding. As a consequence, the NTD of GreB contacts RNAP active center and donates acidic residues that increase the affinity towards a magnesium ion, which is required for cleavage catalysis of the misaligned RNA. These four reconstructions give insights on the catalytic mechanism and dynamics of RNA cleavage and extension. [...]
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37

Burrows, Patricia Clare. "Structure-function studies on the major form of bacterial RNA polymerase." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415040.

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Mitchell, Louise E. "The regulation of RNA polymerase III transcription by protein kinase CK2." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/399/.

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In order for cells to proliferate, a certain size has to be reached, which depends primarily on the rate of translation. RNA polymerase (pol) III plays a key role in protein synthesis by catalysing the production of small, untranslated RNA molecules such as transfer (tRNA) and 5S ribosomal RNA (5S rRNA). Indeed, recent evidence suggests that tRNAiMet production is limiting for translation and proliferation in some cell types. Therefore, the rate of pol III transcription plays a fundamental role in cellular growth and proliferation. Regulation of pol III output is mediated via a number of different mechanisms that can alter the activities of the transcription factors which are responsible for directing pol III transcription. Work presented in this thesis aimed at investigating the mechanisms behind the regulation of pol III transcription by the protein kinase CK2.
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39

Crighton, Diane. "Regulation of RNA polymerase III transcription by the tumour suppessor p53." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252510.

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40

Felton-Edkins, Zoe A. "Deregulation of RNA polymerase III transcription in response to Polyomavirus transformation." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368590.

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41

Blau, Michael Justin. "The regulation of transcription initiation and elongation by RNA polymerase II." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363005.

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42

Yudkovsky, Natalya. "Mechanisms of factor recruitment at promoters during RNA polymerase II transcription /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/5046.

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43

Djupedal, Ingela. "Characterization of RNA polymerase II subunit Rpb7 in silencing and transcription." Stockholm : Department of Biosciences and Nutrition, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-606-4/.

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44

Reeves, Wendy Michele. "Diverse functions of yeast co-activators in RNA polymerase II transcription /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5058.

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Kim, Jaesang. "Isolation and functional characterization of cofactors of RNA polymerase II transcription." Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/40212.

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46

Varshney, Dhaval. "Regulation of RNA polymerase III transcription by DNA methylation and chromatin." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3114/.

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Mammalian genomes contain huge numbers of short interspersed elements (SINEs). An extreme case is provided by the human genome, which carries ~106 copies of Alu SINEs that together account for ~10% of total chromosomal DNA. SINEs spread by retrotransposition, which depends on their transcription by pol III. This transcription is heavily suppressed. Silencing is thought to involve DNA methylation and packaging the SINEs into chromatin structures that deny access of transcription factors. It has been argued that this may be of great importance to prevent SINEs from competing with essential genes for a limited pool of transcription machinery. Our investigation of this has revealed some unexpected findings. This study has also investigated the effects of SWI/SNF chromatin remodellers on tRNA transcription.
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47

Jia, Yiping. "Mechanistic studies of DNA-dependent transcription initiation and RNA synthesis by bacteriophage T7 RNA polymerase /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487953204281995.

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48

Hög, Friederike. "Functional studies of RNA polymerase II recruitment to promoter DNA and impact of BRF1 mutations on RNA polymerase III-dependent transcription." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-179326.

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49

Ciesiolka, Adam. "A proteomic analysis of the dynamic RNA polymerase I complexes." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/7546111a-2cd4-4e04-87fd-da443e83fc85.

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50

Vintermist, Anna. "Chromatin remodelling of ribosomal genes - be bewitched by B-WICH." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-115530.

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Transcription of the ribosomal genes accounts for the majority of transcription in the cell due to the constant high demand for ribosomes. The number of proteins synthesized correlates with an effective ribosomal biogenesis, which is regulated by cell growth and proliferation. In the work presented in this thesis, we have investigated the ribosomal RNA genes 45S and 5S rRNA, which are transcribed by RNA Pol I and RNA Pol III, respectively. The focus of this work is the chromatin remodelling complex B-WICH, which is composed of WSTF, the ATPase SNF2h and NM1. We have studied in particular its role in ribosomal gene transcription. We showed in Study I that B-WICH is required to set the stage at rRNA gene promoters by remodelling the chromatin into an open, transcriptionally active configuration. This results in the binding of histone acetyl transferases to the genes and subsequent histone acetylation, which is needed for ribosomal gene activation. Study II investigated the role of B-WICH in transcription mediated by RNA polymerase III. We showed that B-WICH is essential to create an accessible chromatin atmosphere at 5S rRNA genes, which is compatible with the results obtained in Study 1. In this case, however, B-WICH operates as a licensing factor for c-Myc and the Myc/Max/Mxd network. Study III confirmed the importance and the function of the B-WICH complex as an activator of ribosomal genes. We demonstrated that B-WICH is important for the remodelling of the rDNA chromatin into an active, competent state in response to extracellular stimuli, and that the association of the B-WICH complex to the rRNA gene promoter is regulated by proliferative and metabolic changes in cells. The work presented in this thesis has confirmed that the B-WICH complex is an important regulator and activator of Pol I and Pol III transcription. We conclude that B-WICH is essential for remodelling the rDNA chromatin into a transcriptionally active state, as required for efficient ribosomal gene transcription.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 3: Manuscript.

 

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