Dissertations / Theses on the topic 'Transcription'
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Elzi, David John. "Transcriptional properties of the Kaiso class of transcription factors /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5027.
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Pombo, Ana Maria Pires. "Transcription factories : sites of transcriptional activity in mammalian nuclei." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268165.
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Xie, Yunwei. "Nucleosomes, transcription and transcription regulation in Archaea." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1127830717.
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Thesis (Ph. D.)--Ohio State University, 2005.Title from first page of PDF file. Document formatted into pages; contains xiv, 200 p.; also includes graphics (some col.). Includes bibliographical references (p. 167-197). Available online via OhioLINK's ETD Center
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Xie, Yunwei. "nucleosome, transcription and transcription regulation in Archaea." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1127830717.
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Dennis, Jonathan Hancock. "Transcriptional regulation by Brn 3 POU domain containing transcription factors." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249684.
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Chambers, Anna Louise. "Transcription termination by a transcription-repair coupling factor." Thesis, University of Bristol, 2005. http://hdl.handle.net/1983/b95a2024-73ae-460d-89bf-3c064a780c78.
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Yao, Ya-Li. "Regulation of yy1, a multifunctional transciption [sic] factor /." [Tampa, Fla.] : University of South Florida, 2001. http://purl.fcla.edu/fcla/etd/SFE0000626.
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Brehm, Alexander Jorg Georg. "Octamer-dependent transcriptional activation by the embryonal transcription factor Oct-4." Thesis, Open University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338344.
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Albhilal, Waleed Sulaiman. "The Arabidopsis thaliana heat shock transcription factor A1b transcriptional regulatory network." Thesis, University of Essex, 2015. http://repository.essex.ac.uk/15732/.
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Plants as sessile organisms have adapted highly sophisticated cellular processes to cope with environmental stress conditions, which include the initiation of complex transcriptional regulatory circuits. The heat shock transcription factors (HSFs) have been shown to be central regulators of plant responses to abiotic and biotic stress conditions. However, the extremely high multiplicity in plant HSF families compared to those of other kingdoms and their unique expression patterns and structures suggest that some of them might have evolved to become major regulators of other non-stress related processes. Arabidopsis thaliana HSFA1b (AtHSFA1b) has been shown to be a major regulator of various forms of plant responses to abiotic and biotic stresses. However, it has also been suggested that overexpression of AtHSFA1b results in a subtle developmental effect in Arabidopsis thaliana and Brassica napus in the form of increased seed yield and harvest index. Through genome-wide mapping of the AtHSFA1b binding profile in the Arabidopsis thaliana genome, monitoring changes in the AtHSFA1b-regulated-transcriptome, and functional analysis of AtHSFA1b in Saccharomyces cerevisiae under non-stress and heat stress conditions, this study provides evidence of the association of AtHSFA1b with plant general developmental processes. Furthermore, the outcome of this research shows that AtHSFA1b controls a transcriptional regulatory network operating in a hierarchical manner. However, in an agreement with a previously suggested model, the results from this study demonstrate that the involvement of AtHSFA1b in the regulation of heat stress response in Arabidopsis thaliana is possibly limited to the immediate and very early phases of heat stress response which also results in a collapse in its transcriptional network which seems to be accompanied by a general shutdown in plant growth and development.
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Kwek, Kon Yew. "Regulation of general transcription factor IIH (TFIIH) in transcription." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427628.
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Toedling, Joern Michael. "Comprehensive analysis of high-throughput experiments for investigating transcription and transcriptional regulation." Thesis, University of Cambridge, 2009. https://www.repository.cam.ac.uk/handle/1810/267885.
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As the number of fully sequenced genomes grows, efforts are shifted towards investigation of functional aspects. One research focus is the transcriptome, the set of all transcribed genomic features. We aspire to understand what features constitute the transcriptome, in which context these are transcribed and how their transcription is regulated. Studies that aim to answer these questions frequently make use of high-throughput technologies that allow for investigation of multiple genomic regions, or transcribed copies of genomic regions, in parallel. In this dissertation, I present three high-throughput studies I have been involved in, in which data gained from oligo-nucleotide tiling microarrays or large-scale cDNA sequencing provided insights into the transcriptome and transcriptional regulation in the model organisms Saccharomyces cerevisiae and Mus musculus. Interpretation of such high-throughput data poses two major computational tasks. The primary statistical analysis includes quality assessment, data normalisation and identification of significantly affected targets, i.e. regions of the genome deemed transcribed or involved in transcriptional regulation. Second, in an integrative bioinformatic analysis, the identified targets need to be interpreted in context of the current genome annotation and related experimental results. I provide details of these individual steps as they were conducted in the three studies. For both primary and integrative analysis, functional, extensible and welldocumented software is required, which implements individual analysis steps, allows for concise visualisation of intermittent and final results and facilitates the construction of automated, programmed workflows. Ideally such software is optimised with respect to scalability, reproducibility and methodical scope of the analyses. This dissertation contains details of two such software packages in the Bioconductor project, which I (co-)developed.
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Truscott, Mary. "The molecular basis of transcriptional activation by the CDP/Cux transcription factor /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103187.
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The CDP/Cux transcription factor is expressed as a 200 kDa protein that interacts rapidly and transiently with DNA. Proteolytic processing generates a shorter isoform, p110 CDP/Cux, that binds stably to DNA. Processing occurs at the G1/S transition of the cell cycle in normal cells, and constitutively in transformed cells. p110 CDP/Cux stimulates cell proliferation by accelerating entry into S phase. Transgenic mice expressing p110 CDP/Cux are more susceptible to different cancers.CDP/Cux was originally described as a repressor of transcription. My goal was to verify whether CDP/Cux might also participate in transcriptional activation and characterize the molecular basis for transcriptional activation by CDP/Cux. Using the DNA polymerase alpha gene promoter as a model system, I showed that stimulation of a DNA pol alpha reporter correlated with DNA binding. Importantly, p110 CDP/Cux stimulated expression from the endogenous DNA pol alpha promoter. Linker-scanning analysis of the DNA pol alpha promoter identified a cis-element that was required for p110-mediated activation, yet was not bound by it. I determined that E2F1 and E2F2 cooperated with p110 in activating the DNA pol alpha promoter, and did so via this cis-element. Furthermore, CDP/Cux recruited these E2Fs to the promoter in chromatin immunoprecipitation experiments. Location array analysis revealed many targets common to p110 and E2F1. DNA metabolism and cell cycle targets were overrepresented, and further studies showed that p110 and E2F cooperated to activate many cell cycle genes.
I also described a second proteolytic event, which generated an isoform lacking two active repression domains in the C-terminus. Processing was observed in S phase, but not in early G1, suggesting that processing occurs in proliferating cells. I determined that caspases were responsible for this processing, and that this occurs in non-apoptotic conditions. A C-terminally-truncated CDP/Cux protein was a more potent activator of cell cycle-regulated promoters, and accelerated entry of Kit225 T cells into S phase, while uncleavable p110 CDP/Cux proteins were inactive in both assays. These results identified p110 CDP/Cux as a substrate of caspases in proliferating cells, and suggested a mechanism by which caspases may accelerate cell cycle progression.
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Ching, Chi-yun Johannes, and 程子忻. "Transcriptional regulation of p16INK4a expression by the forkhead box transcription factor FOXM1." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29466192.
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Cusack, Martin. "The role of DNA methylation on transcription factor occupancy and transcriptional activity." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:7d0b7fe7-dee1-433f-8656-c9ee2a216d48.
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DNA methylation is an epigenetic mark that is deposited throughout the genome of mammals and plays an important role in the maintenance of transcriptionally repressive states across cell divisions. There are two major mechanisms by which DNA methylation has been proposed to act: one involves the recognition of the mark by protein complexes containing histone deacetylases (HDACs) that can remodel the local chromatin. Alternatively, methylation has been suggested to directly affect the interaction between transcription factors and their cognate binding sequence. The aim of this research was to determine the contributions of these two mechanisms in cells. The importance of HDAC activity in mediating DNA methylation-dependent transcriptional repression was assessed by comparing the genes and retrotransposons that are upregulated in response to DNA methylation loss or the disruption of HDAC activity. To this purpose, we performed whole-genome transcriptional analysis in wild type and DNA methylation-deficient mouse embryonic stem cells (DNMT.TKO mESCs) in the presence and absence of the HDAC inhibitor trichostatin A. Our data suggests that there are few genes whose repression is solely dependent on the recruitment of HDACs by DNA methylation in mESCs. Rather it appears that DNA methylation and HDAC-mediated silencing represent two independent layers of repression that converge at certain transcriptional elements. To investigate the contribution of DNA methylation on the genome-wide occupancy of transcription factors, we compared the global chromatin accessibility landscape and the binding profile of candidate transcription factors in the absence or presence of DNA methylation. We found that loss of DNA methylation associates with localised gains in accessibility, some of which can be linked to the novel binding of transcription factors such as GABPA, MAX, NRF1 and YY1. Altogether, our results present new insights into the interplay between DNA methylation and histone deacetylation and their impact on the localisation of transcription factors from different families.
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Xu, Meng. "Specialised transcription factories." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:a41d3243-c233-491a-916b-4e329cace434.
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The intimate relationship between the higher-order chromatin organisation and the regulation of gene expression is increasingly attracting attention in the scientific community. Thanks to high-resolution microscopy, genome-wide molecular biology tools (3C, ChIP-on-chip), and bioinformatics, detailed structures of chromatin loops, territories, and nuclear domains are gradually emerging. However, to fully reveal a comprehensive map of nuclear organisation, some fundamental questions remain to be answered in order to fit all the pieces of the jigsaw together. The underlying mechanisms, precisely organising the interaction of the different parts of chromatin need to be understood. Previous work in our lab hypothesised and verified the “transcription factory” model for the organisation of mammalian genomes. It is widely assumed that active polymerases track along their templates as they make RNA. However, after allowing engaged polymerases to extend their transcripts in tagged precursors (e.g., Br-U or Br-UTP), and immunolabelling the now-tagged nascent RNA, active transcription units are found to be clustered in nuclei, in small and numerous sites we call “transcription factories”. Previous work suggested the transcription machinery acts both as an enzyme as well as a molecular tie that maintains chromatin loops, and the different classes of polymerases are concentrated in their own dedicated factories. This thesis aims to further characterise transcription factories. Different genes are transcribed by different classes of RNA polymerase (i.e., I, II, or III), and the resulting transcripts are processed differently (e.g., some are capped, others spliced). Do factories specialise in transcribing particular subsets of genes? This thesis developed a method using replicating minichromosomes as probes to examine whether transcription occurs in factories, and whether factories specialise in transcribing particular sets of genes. Plasmids encoding the SV40 origin of replication are transfected into COS-7 cells, where they are assembled into minichromosomes. Using RNA fluorescence in situ hybridisation (FISH), sites where minichromosomes are transcribed are visualised as discrete foci, which specialise in transcribing different groups of genes. Polymerases I, II, and III units have their own dedicated factories, and different polymerase II promoters and the presence of an intron determine the nuclear location of transcription. Using chromosome conformation capture (3C), minichromosomes with similar promoters are found in close proximity. They are also found close to similar endogenous promoters and so are likely to share factories with them. In the second part of this thesis, I used RNA FISH to confirm results obtained by tiling microarrays. Addition of tumour necrosis factor alpha (TNF alpha) to human umbilical vein endothelial cells induces an inflammatory response and the transcription of a selected sub-set of genes. My collaborators used tiling arrays to demonstrate a wave of transcription that swept along selected long genes on stimulation. RNA FISH confirmed these results, and that long introns are co-transcriptionally spliced. Results are consistent with one polymerase being engaged on an allele at any time, and with a major checkpoint that regulates polymerase escape from the first few thousand nucleotides into the long gene.
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Young, David Alan. "Plant mitochondrial transcription." Thesis, University of East Anglia, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338216.
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Tucker, Nicholas Peter. "Regulation of transcription by the nitric oxide sensing transcription factor NorR." Thesis, University of East Anglia, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426424.
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Lin, Charles Yang. "c-Myc regulates transcriptional pause release and is a global amplifier of transcription." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/77782.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Computational and Systems Biology Program, 2012.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 203-226).
Elevated expression of the c-Myc transcription factor occurs frequently in human cancers and is associated with tumor aggression and poor clinical outcome. However, the predominant mechanism by which c-Myc regulates global transcription in both healthy and tumor cells is poorly understood. In this thesis, I present evidence that c-Myc is a global regulator of RNA Polymerase II (RNA Pol II) transcriptional pause release. Transcriptional pausing occurs when additional regulatory steps are required to promote elongation of genes after transcription has initiated. Chapter 2 identifies transcriptional pausing as a general feature of transcription by RNA Pol II in mammalian cells. c-Myc is identified as having a major role in promoting release from pause at its target genes. Chapter 3 finds in tumor cells with elevated c-Myc, the transcription factor binds to promoters and enhancers of most actively transcribed genes. The predominant effect of c-Myc binding is to produce higher levels of transcription by promoting RNA Pol II transcriptional pause release. Thus, c-Myc accumulates in the promoter regions of active genes across the cancer cell genome and causes transcriptional amplification, producing increased levels of transcripts within the cells gene expression program. These results imply that transcriptional amplification can reduce rate-limiting constraints for tumor cell growth and proliferation.
by Charles Yang Lin.
Ph.D.
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SICILIANO, DILETTA. "ANALYSIS OF THE TRANSCRIPTIONAL REGULATION OF MTORC1 ACTIVITY BY MIT/TFE TRANSCRIPTION FACTORS." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/607642.
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The mechanistic Target Of Rapamycin Complex 1 (mTORC1) regulates cellular biosynthetic pathways in response to variations in nutrient availability. Activation of mTORC1 is mediated by Rag GTPases, that act as heterodimers and promote mTORC1 recruitment to the lysosome. Many studies have clarified the post-translational control of mTORC1, but little is known about its transcriptional regulation. Our study demonstrates that TFEB, TFE3 and MITF, members of the MiT/TFE family of transcription factors and master regulators of lysosomal and melanosomal biogenesis and autophagy, are nutrient-sensitive transcriptional activators of mTORC1 signaling. During starvation they induce the expression of the RagD gene and this enhances mTORC1 recruitment to the lysosome and its reactivation when nutrients become available. Thus, in periods of nutrient deprivation, this mechanism allows the cell to rapidly reactivate anabolic pathways and turn off catabolism when nutrient levels are restored. Furthermore this mechanism plays an important role in cancer growth. Up-regulation of the MiT/TFE genes in renal cell carcinoma and melanoma is associated to RagD-induced mTORC1 activation, causing cell hyperproliferation and cancer progression.
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Immarigeon, Clément. "Role of mediator complex subunits in transcriptional regulation by GATA and FOG transcription factors during Drosophila development." Toulouse 3, 2014. http://thesesups.ups-tlse.fr/2654/.
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Un enjeu majeur en Biologie est de comprendre comment les milliers de gènes composant le génome sont contrôlés afin d'être exprimés dans les bonnes cellules au bon moment. Cette régulation a lieu en grande partie à l'étape de pré-initiation de la transcription. Ce processus résulte de l'action concertée de nombreuses protéines, dont le complexe Médiateur (MED, ~30 sous-unités protéiques ou SU, >1,5MDa) qui joue un rôle conservé dans la régulation de la transcription des gènes par l'ARN Polymérase II (PolII), de la levure à l'Homme. Ce complexe se lie simultanément à la PolII et aux facteurs de transcription spécifiques (FT). Les FT reconnaissent et se fixent à des séquences régulatrices d'ADN, et dirigent l'expression de leurs gènes-cibles au cours du développement. Le complexe MED, ubiquitaire dans les cellules eucaryotes, semble intégrer le " code des FT " spécifique à chaque cellule, et réguler en conséquence le recrutement et l'activité de la PolII au promoteur des gènes-cibles des FT. La drosophile est un organisme modèle fournissant des outils génétiques puissants pour répondre à des questions biologiques importantes in vivo, notamment concernant la transcription génique. Une famille de FT, les GATA, est impliquée dans des processus développementaux similaires chez les mammifères et la mouche. Ils activent et répriment la transcription, selon le gène considéré et la présence de certains cofacteurs comme les protéines FOG. Le travail présenté ici vise à comprendre comment les FT GATA utilisent le MED pour réguler la transcription de leurs gènes cibles, positivement et négativement. Au cours de ce travail, nous avons généré les premières lignées mutantes pour le gène Med1, et entrepris la caractérisation des fonctions de la SU Med1, connue pour être un cofacteur des FT GATA chez les vertébrés. Nous avons montré que certaines SU MED (dont Med1, 12, 13, 15 et 19) sont impliquées dans des processus dépendant des GATA, tels que l'hématopoïèse, la morphogénèse du notum et la formation des soies mécanosensorielles dorso-centrales. Les deux derniers dépendent du FT GATA Pannier (Pnr) qui, seul, active la transcription des gènes pro-neuraux ac-sc, ou la réprime en présence de son partenaire FOG U-shaped (Ush). Des analyses clonales in vivo ont révélé que Med1, Med15 et Med19, ainsi que Med12 et Med13 appartenant au module détachable CDK8, sont critiques pour l'activation d'ac-sc de façon cellulaire-autonome, suggérant un lien fonctionnel avec Pnr. De manière intéressante, CycC et Cdk8 du module CDK8 ne sont pas requises pour l'activation d'ac-sc, mais sont requises pour sa répression dans les cellules voisines, soulignant la diversité d'action des SU MED in vivo. Med19 interagit physiquement avec Pnr, et pourrait donc être le point d'ancrage par lequel Pnr recrute le MED pour activer la transcription. De plus, le facteur FOG Ush inhibe l'interaction Med19-Pnr en formant un hétérodimère Pnr-Ush. La compétition pour se fixer à Pnr entre Med19 (co-activateur) et Ush (co-répresseur) pourrait expliquer les actions antagonistes de Pnr sur ses gènes-cibles. Med19 est également requise pour la transactivation par un autre GATA : Serpent (Srp, cf. Gobert et al. 2010). Nous montrons ici que Med19 interagit également avec Srp, suggérant que Med19 pourrait être un cofacteur général des GATA, alors que Med1 ne semble pas avoir d'affinité pour les GATA chez la drosophile (contrairement à la SU Med1 chez les mammifères). Cela soulève des questions quant à la manière par laquelle les interactions entre FT et SU MED apparaissent, puis sont conservées, ou non, au cours l'évolution. Ces résultats mettent en lumière des interactions croisées entre Med19, GATA-Pnr et FOG-Ush qui permettent de comprendre mécanistiquement comment Pnr active et réprime la transcription. Ce travail représente une étape importante pour la compréhension de la façon dont les combinatoires de FT sont intégrées par le MED pour aboutir à une régulation fine de la transcriptionA major aim of today's research in Biology is to understand how the thousands of genes composing the genome are regulated in order to be expressed in the right cells at the right time. This regulation occurs in large part before gene transcription, at the pre-initiation step. This process results of the concerted action of many proteins, including the large Mediator complex (MED, ~30 protein subunits, >1. 5 MDa), which plays a conserved and crucial role in the regulation of protein-coding genes transcription by RNA polymerase II (PolII), from yeast to humans. This modular complex makes direct core contacts with PolII and general transcription factors, while some subunits can bind to DNA-bound specific transcription factors (TFs). TFs recognize and bind specific regulatory DNA sequences, and drive the tissue-specific expression of their target genes during development. The ubiquitously expressed MED is thought to integrate a cell-specific STF "code" to regulate PolII recruitment and activity at gene promoters. Drosophila melanogaster is a valuable animal model that provides many genetic tools - such as mutant strains and transgenic lines - to address important biological questions in vivo, such as how gene transcription is regulated. A family of TFs, the GATAs, is involved in diverse developmental processes in both Drosophila and vertebrates. They are both activator and repressor TFs, depending on the target gene and the available cofactors, such as Friend Of GATA (FOG) family proteins. The work presented here aimed to understand how GATA TFs use the MED to regulate their target genes both positively and negatively. During the course of this work we generated the first Drosophila mutants for Med1, and investigated the functions of this important subunit in vivo, known as a cofactor of GATAs in vertebrates. We identified a subset of Drosophila MED subunits (including Med1, 12, 13, 15, 19) which are required for proper GATA-dependent processes, such as haematopoiesis, notum morphogenesis and dorso-central (DC) mechanosensory bristle emergence. The last two processes depend on Pannier (Pnr), a GATA-type TF, which directly activates achaete-scute (ac-sc) proneural genes transcription singly, and represses it in presence of its FOG partner U-shaped (Ush). Clonal analysis in vivo showed that Med1, Med15 and Med19, along with Med12/13 subunits of the detachable "CDK8" module of the MED, are critical for ac-sc activation in a cell-autonomous manner, suggesting functional interactions with Pnr. Interestingly, CycC and Cdk8 subunits from CDK8 module are not involved in ac-sc activation, but are required to ensure ac-sc inhibition in surrounding cells, underscoring the diversity of MED subunits functions in vivo. Moreover, we show that Med19 binds physically to Pnr. Thus, Med19 might be the anchor point by which Pnr recruits the MED at Pnr-activated genes. Furthermore, the FOG factor U-shaped inhibits Med19-Pannier interaction by heterodimerizing with Pannier. Thus, the competition for Pnr binding between Med19 (coactivator) and Ush (corepressor) could be responsible for the antagonistic roles of Pnr on the transcription of its target genes. Interestingly, Med19 is also required for transactivation by another GATA factor: Serpent (Srp, cf. Gobert et al. , 2010). Here we show that Med19 also interacts physically with Srp, suggesting that Med19 could be a general cofactor of GATAs in drosophila. On the other hand, Med1 showed no affinity for Drosophila GATAs (contrary to vertebrate Med1), raising questions about the way MED-TF interactions are acquired and maintained, or not, during evolution. This work highlights the interplay between Med19, GATA-Pnr and FOG-Ush, allowing a mechanistic understanding of Pnr actions as both an activator and a repressor of gene transcription. This PhD thesis is an important step towards appreciating how combinatorial codes of TFs are integrated by the MED to regulate gene transcription during development
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Talvik, Gertrud. "Transcription regulation in Plasmodium falciparum : functional characterisation of general transcription factor IIB." Master's thesis, University of Cape Town, 2016. http://hdl.handle.net/11427/20616.
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Plasmodium falciparum is the causative agent of the most severe form of malaria and continues to pose challenges to international healthcare, with high mortality rates and emergence of drug-resistant strains. Plasmodium falciparum has multiple sexual and asexual lifecycle stages within its Anopheline mosquito and human hosts, accompanied by distinct morphological changes. The complex lifecycle, along with the ability to adjust rapidly to different environmental niches, is governed by highly regulated and tightly synchronised changes in stage-specific gene expression. In eukaryotes, regulation of RNA Polymerase II transcription initiation is one of the main mechanism of gene expression control. Past research has revealed the presence of crucial elements of RNA Polymerase II (RNAPII) transcription machinery in P. falciparum, however, the precise transcription initiation mechanisms in P. falciparum remain to date undescribed. Bioinformatics studies have found very little homology between human and P. falciparum transcription factors. Furthermore, because of the extreme bias toward A/T in the Plasmodium genome, TATA-box and other core promoter elements that direct transcription initiation, cannot be determined with confidence in bioinformatics studies. Functional characterisation of the key protein factors involved in transcription initiation is a first important step towards the identification of core promoter elements and could reveal currently unknown eukaryotic transcription initiation mechanisms or new anti-malarial targets. In eukaryotes, TATA-binding protein (TBP) and transcription factor IIB (TFIIB) are the key protein factors involved in the core promoter recognition and RNAPII preinitiation complex (PIC) assembly. TBP nucleates PIC assembly by binding the TATA box, thereafter the TBP-TATA complex is further stabilised by TFIIB. In addition, TFIIB has a crucial role in RNAPII recruitment and transcription start site selection and is therefore deemed indispensable in eukaryotic transcription. P. falciparum TBP is the only PIC component in P. falciparum that has been functionally characterised to date, albeit to a very limited extent. This research study reports the successful expression and purification, as well as initial characterisation of DNA-binding activity of P. falciparum TBP and TFIIB. We observe PfTBP binding at multiple locations on putative P. falciparum promoters. We further report PfTBP-independent binding activity of PfTFIIB, that has not been previously observed under the conditions and has implications for novel DNA-binding mechanisms of PfTFIIB. Furthermore, we conclusively demonstrate the formation of a PfTBP-PfTFIIB-promoter ternary complex.
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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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Li, Yuxin. "The DEC1 transcription factor : oncogenic involvement and molecular mechanisms on transcription regulation /." View online ; access limited to URI, 2003. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3115632.
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Johansson, Kajsa. "Transcription of Historical Encrypted Manuscripts : Evaluation of an automatic interactive transcription tool." Thesis, Uppsala universitet, Institutionen för lingvistik och filologi, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-385254.
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Countless of historical sources are saved in national libraries and archives all over the world and contain important information about our history. Some of these sources are encrypted to prevent people from reading it. This thesis examines a semi-automated Interactive transcription Tool based on unsupervised learning without any labelled training data that has been developed for transcription of encrypted sources and compares it to manual transcription. The interactive transcription tool is based on handwritten text recognition techniques and the system identifies cluster of symbols based on similarity measures. The tool is evaluated on ciphers with number sequences that have previously been transcribed manually to compare how well the transcription tool performs. The weaknesses of the tool are described and suggestions on how the tool can be improved are proposed. Transcription based on HTR techniques and clustering shows promising results and the unsupervised method based on clustering should be further investigated on ciphers with various symbol sets.
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Sydow, Jasmin F. "Structural basis of transcription." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-107071.
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Min, Mi-Kyung. "Baculovirus vector transcription analyses." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279873.
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Rennick, L. J. "Transcription attenuation in morbilliviruses." Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403206.
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Hennigan, Aidan Noel. "Transcription in Methanococcus vannielii /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487841975356207.
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An, Sungwhan. "Mechanism of coronavirus transcription /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
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Ferrara, Giovanni Antonio. "Studies of transcriptional regulation by the vitamin D3 receptor and cAMP-responsive transcription factors." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69734.
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Cells of complex organisms communicate with each other by sending molecular signals. These signals can be classified by their solubility properties. Hydrophilic signals, in the form of peptides or small hydrophilic molecules, interact with extracellular receptors located on the surface of target cells. Binding of ligand to its receptor leads to transduction of an intracellular signal via a second messenger. Lipophilic signals (steroids, vitamin D$ sb3$, thyroid hormone, and retinoids) traverse the plasma membrane and bind to specific intracellular proteins, known collectively as nuclear receptors, rendering them active. These ligand-receptor complexes then regulate the transcription of target genes. In this thesis, transcriptional regulation by two different systems has been studied. First, recent evidence suggests that expression of the parathyroid hormone-related peptide (PTHrP) gene is sensitive to elevated levels of cyclic adenosine monophosphate (cAMP). Second, vitamin D$ sb3$ is activated in the kidney by hydroxylation and functions by diffusing across the plasma membrane of target cells and binding the vitamin D$ sb3$ receptor (VDR). (Abstract shortened by UMI.)
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Kiosses, Theodore. "DNA binding specificity and transcriptional regulation of Six4 : a myotonic dystrophy associated transcription factor." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3948.
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Attaining an understanding of the mechanisms underpinning development has been amongst the cardinal scientific challenges of our age. The transition from a single cell organism to the level of complexity evidenced in higher eukaryotes has been facilitated by the advent of intricate developmental networks involving a plethora of factors that synergise to allow for precise spatio-temporal expression of the proteins present in higher organisms. Development is often portrayed as a domino like cascade of events stemming from relatively uncomplicated origins that go on to branch out and form associations and interactions amongst multitudinous actors that will inexorably lead towards a higher state of order. Transcription factors occupy a central position within this tapestry of interactions. They regulate expression of the various required proteins and they provide the cues for the developmental events that will eventually shape an organism. These factors frequently remain unknown until some occurrence causes developmental processes to fail and inadvertently focus attention on the factors that facilitate development. Myotonic dystrophy is a useful paradigm of such a developmental dysfunction that has led to the discovery of a transcription factor integral to both muscle development and gonadogenesis in both Drosophila and higher eukaryotes.
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Rheinheimer, Brenna Ann. "Alternative Transcription Of The SLIT2/Mir-218-1 Transcriptional Axis Mediates Pancreatic Cancer Invasion." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/605118.
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The development of several organ systems through modeling and shaping of the tissue structure occurs from signaling through axon guidance molecules. The Slit family of ligands has been shown to regulate branching morphogenesis in mammary gland duct development and loss of Slit gene expression during this time leads to the formation of hyperplastic, disorganized lesions suggesting a potential role for Slits in cancer formation. Characterization of human pancreatic ductal adenocarcinoma cell lines showed a loss of SLIT2 expression in cells that contain activated Kras. Loss of SLIT2 expression was associated with DNA methylation of CpG sites within the SLIT2 core promoter and chromatin enrichment of repressive histone modifications at the SLIT2 transcriptional start site. Additionally, treatment of pancreatic ductal adenocarcinoma cell lines with demethylating agent 5-aza-2'-deoxycytidine led to SLIT2 re-expression while treatment with histone deacetylase inhibitor Trichostatin A did not. Mir-218-1 is an intronic microRNA encoded within intron 15 of the SLIT2 gene. Expression of mir-218-1 does not correlate with SLIT2 mRNA expression suggesting that it is transcribed from a promoter independent of the SLIT2 gene promoter. Pancreatic ductal adenocarcinoma cell lines showed a peak of H3K4me3 chromatin enrichment localized to a 1kb region within intron 4 of the SLIT2 gene denoting a candidate alternative promoter for mir-218-1. A concordant peak of H4ac chromatin enrichment overlapped the peak of H3K4me3 enrichment and transcriptional activity was measured from the 1kb region in all pancreatic ductal adenocarcinoma cell lines. A NF-κB binding site was also predicted to exist within the 1kb region. Transfection with two independent siRNAs to NF-κB led to an increase in both pre-mir-218-1 and mature mir-218-1 while treatment with an inhibitor to IκB kinase led to an increase in pre-mir-218-1 expression. Additionally, the p65 subunit of NF-κB was found to bind to the candidate mir-218-1 alternative promoter in pancreatic ductal adenocarcinoma cell lines that do not contain DNA CpG methylation at the predicted NF-κB binding site. It was discovered that miR-218 is a modulator of ARF6 expression suggesting a role in the inhibition of pancreatic ductal adenocarcinoma cell invasion through modulation of the actin cytoskeleton. Overexpression with a miR-218 precursor showed that miR-218 is an inhibitor of pancreatic ductal adenocarcinoma cell invasion in two dimensions. Additionally, it was found that while miR-218 does not have an affect on the ability of pancreatic ductal adenocarcinoma cells to form functional invadopodia, miR-218 is an inhibitor of the extracellular matrix degradation properties of mature invadopodia. Interestingly, the effect of miR-218 on pancreatic ductal adenocarcinoma cell invasion or extracellular matrix degradation is not reliant on the cell's dependency on Kras signaling for growth and survival. Collectively, these observations indicate that understanding the transcriptional regulation of SLIT2 and mir-218-1 expression as well as their signaling properties may provide a step toward the development of diagnostic tests and therapeutic treatments for patients with invasive or metastatic pancreatic ductal adenocarcinoma.
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Smith, Richard LeRoy. "Cis-regulatory Sequence and Co-regulatory Transcription Factor Functions in ERα-Mediated Transcriptional Repression." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2261.
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Estrogens exert numerous actions throughout the human body, targeting healthy tissue while also enhancing the proliferative capacity of breast cancers. Estrogen signaling is mediated by the estrogen receptor (ER), which binds DNA and ultimately affects the expression of adjacent genes. Current understanding of ER-mediated transcriptional regulation is mostly limited to genes whose transcript levels increase following estrogen exposure, though recent studies demonstrate that direct down-regulation of estrogen-responsive genes is also a significant feature of ER action. We hypothesized that differences in cis-regulatory DNA was a factor in determining target gene expression and performed computational and experimental studies to test this hypothesis. From our in silico analyses, we show that the binding motifs for certain transcription factors are enriched in cis-regulatory sequences adjacent to repressed target genes compared to induced target genes, including the motif for RUNX1. In silico analyses were tested experimentally using dual luciferase reporter assays, which indicate that several ER binding sites are estrogen responsive. Mutagenesis of transcription factor motifs (for ER and RUNX1) reduced the response of reporter gene. Further experiments demonstrated that co-recruitment of ER and RUNX1 is necessary for repression of gene expression at some target genes. These findings highlight a novel interaction between ER and RUNX1 and their role in transcriptional repression in breast cancer.
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Chery, Alicia. "Rôle de la transcription pervasive antisens chez Saccharomyces cerevisiae dans la régulation de l'expression des gènes." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066191/document.
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L'expression des gènes est finement régulée dans la cellule et soumise à de multiples contrôles-qualité. Cette régulation intervient à différents niveaux, de façon à garantir une synthèse efficace des produits fonctionnels de l'expression génique, et pour assurer une adaptation à un changement environnemental. Notamment, les régulations transcriptionnelles sont cruciales pour contrôler la cinétique et le niveau d'expression des gènes. La transcription pervasive est une transcription généralisée non-codante et instable qui fut révélée chez la levure Saccharomyces cerevisiae. Bien que son potentiel régulateur ait été démontré de façon ponctuelle, la question de sa fonctionnalité globale restait ouverte. Lors de ma thèse, j'ai pu montrer l'existence de phénomènes multiples d'interférence transcriptionnelle liés à la transcription pervasive, pour co-réguler un ensemble de gènes entre la phase exponentielle et la quiescence. En effet, la transcription non-codante en antisens des gènes concernés conduit à leur répression, dans des conditions où ils ne doivent pas être exprimés. Le mécanisme de répression fait intervenir des modifications de la chromatine. La levure bourgeonnante, dépourvue de la machinerie d'ARN interférence, présente donc un système fin de régulation de l'expression génique utilisant la transcription pervasiveIn the cell, gene expression is finely tuned and is submitted to different quality-controls. Gene are regulated at different expression levels in order to guarantee a proper synthesis of functional products, and to ensure an optimal adaptation to environmental changes. In particular, transcriptional regulations are critical for gene expression level and kinetics.Pervasive transcription, defined as a generalized non-coding and unstable transcription, was discovered in the yeast Saccharomyces cerevisiae. Although its regulatory potential was punctually shown, the question of its global functionality still remained. During my PhD, I could show the existence of numerous transcriptional interference mechanisms involved in the co-regulation of a group of genes between exponential phase and quiescence. Indeed, non-coding transcription in antisense to genes promoter leads to its repression in conditions where they have to be switched off. The repression mechanism is allowed by chromatin modifications.Hence, budding yeast that lacks RNA interference machinery has developed a fine regulation system using pervasive transcription
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Qingquan, Liu. "Investigating the mechanisms of growth factor independence-1 (Gfi-1)-mediated transcriptional repression of p21Cip1 and MBP." Toledo, Ohio : University of Toledo, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1241726388.
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Dissertation (Ph.D.)--University of Toledo, 2009.Typescript. "Submitted as partial fulfillment of the requirements for The Doctor of Philosophy in Biology." "A dissertation entitled"--at head of title. Title from title page of PDF document. Bibliography: p. 84-97.
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Zandvakili, Arya. "The Role of Affinity and Arrangement of Transcription Factor Binding Sites in Determining Hox-regulated Gene Expression Patterns." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535708748728472.
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Ngondo, Richard Patryk. "Caractérisation du potentiel régulateur du facteur de transcription ZNF143." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ078.
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Des données suggéraient que le facteur de transcription ZNF143 régule l’expression de milliers de gènes mais très peu d’informations étaient disponibles sur les gènes cibles, réseaux de gènes, processus biologiques et mécanismes impliquant ZNF143. Pour mon travail de thèse je me suis intéressé au potentiel régulateur de ce facteur en particulier chez l’homme. Mon projet de recherche a premièrement consisté à identifier toutes les cibles génomiques de ZFN143 puis à caractériser fonctionnellement cet interactome. Les résultats obtenus ont permis d’identifier plus de 3000 gènes cibles de ZNF143, principalement impliqués dans des processus liés à la croissance cellulaire. Mes travaux ont aussi permis de mettre à jour de nouveaux mécanismes de régulation impliquant ce facteur. En effet, nous avons démontré que les facteurs de transcription ZNF143, THAP11 et Notch1 modulent l’expression d’un répertoire commun de gènes via des sites de liaison à l’ADN chevauchant. Nous avons aussi montré que ZNF143 joue un rôle essentiel dans l’expression des gènes dirigés par des promoteurs bidirectionnels et qu’il est aussi impliqué dans une boucle d’autorégulation transcriptionnelle de son expressionNumerous data were suggesting that the transcription factor ZNF143 regulates the expression of thousand of genes. However, nothing was known about the genome wide regulatory networks, biological processes and transcriptional mechanisms involving this factor.For my PhD thesis I was interested in exploring the regulatory potential of the ZNF143 transcription factor in human. The goal of my project was to identify all the genomic targets of this factor and functionally characterize this ZNF143-DNA interactome. The results I obtained allowed us to identify more than 3000 genes targeted by ZNF143, mainly involved in biological processes linked to cell proliferation. My work also led us to discover new transcriptional mechanisms involving ZNF143. We demonstrated that the transcription factors ZNF143, THAP11 and Notch1 modulate the expression of a common set f gene via overlapping DNA binding sites. Moreover, we also showed that ZNF143 in essential for the divergent expression of genes from bidirectional promoters and that its expression is regulated through auto-regulatory feedback loop
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MacKinnon-Roy, Christine. "The role of transcription elongation factor IIS in transcription-coupled nucleotide excision repair." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28454.
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Transcription-coupled nucleotide excision repair (TC-NER) removes bulky DNA lesions from the template strand at actively transcribed genes. The RNA polymerase II (RNAPII) holoenzyme complex forms a stable ternary complex at the site of DNA damage which may block access of DNA repair proteins to the site of DNA lesions. Therefore, there is considerable interest in understanding how repair is coupled to transcription. Based on elegant in vitro studies, it has been hypothesized that transcription elongation factor IIS (TFIIS), by catalyzing the reverse translocation of RNAPII, may allow access of DNA repair proteins to sites of DNA damage. Here, we tested this hypothesis by assessing TC-NER capacity in cells in which TFIIS expression has been reduced by RNA interference. Surprisingly, we found that decreased TFIIS levels did not affect the repair of transcription-blocking DNA lesions and did not affect the sensitivity of targeted cells to UV light or cisplatin. These results do not support a role for TFIIS in TC-NER. We conclude conservatively that TFIIS levels are not limiting for TC-NER.
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Barthel, Kristen Kara Bjorkman. "Mammalian strategies to regulate transcription: Transcription factor sumoylation and cis-regulatory region identification." Connect to online resource, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3284477.
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Trevett, Julie A. "Teacher-transcription and self-transcription as aids for teaching and learning jazz improvisation." Thesis, University of Exeter, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421583.
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Roberts, Karen. "Regulation of melanocyte-specific transcription by the transcription factors BRN-2 and microphthalmia." Thesis, Institute of Cancer Research (University Of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286144.
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Briand, Jean-Baptiste. "Etude du contrôle de la transcription envahissante par la terminaison de la transcription." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA112079/document.
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La terminaison de la transcription est essentielle, aussi bien pour assurer la formation de l’extrémité 3’ de transcrits fonctionnels que pour éviter les phénomènes d’interférence transcriptionnelle entre des régions transcrites adjacentes. Ceci est particulièrement important dans un génome compact comme celui de S. cerevisiae. La terminaison est aussi l’une des stratégies principales que la cellule emploie pour contrôler et limiter la transcription dite envahissante ou cachée. Chez S. cerevisiae, l’ARN polymérase II est responsable de la transcription des ARNm et de nombreuses classes d’ARN non codants tels que les sn(o)ARN et les CUT (Cryptic Unstable Transcripts). Ces derniers représentent une fraction importante des transcrits issus de la transcription cachée. Il existe deux voies canoniques de terminaison de la transcription par cette polymérase. Elles font intervenir le complexe de clivage et de polyadénylation, CPF-CF, notamment pour la terminaison des ARNm ou le complexe NNS pour la terminaison des sn(o)ARN et des CUT. Au cours de ma thèse j’ai étudié deux aspects de la terminaison de la transcription : 1) l’étude des motifs de recrutement du complexe NNS et 2) l’identification et la caractérisation d’une nouvelle voie de terminaison par le facteur Rap1. Les complexes CPF-CF et NNS agissent tous les deux en liant le transcrit naissant et l’ARN pol II. Le complexe NNS lie l’ARN naissant grâce à ses sous-unités Nrd1 et Nab3 qui reconnaissent des motifs spécifiques. Cependant, bien que la séquence de ces motifs soit maintenant connue, leur présence ne permet pas de définir de façon certaine un terminateur. En effet, le nombre de ces motifs varie beaucoup d’un terminateur à l’autre. Afin de mieux comprendre la structure des terminateurs ciblés par le complexe NNS et l’organisation des motifs liés par Nrd1 et Nab3, j’ai recherché les séquences impliquées dans la terminaison d’un CUT modèle en réalisant une mutagenèse aléatoire et j’ai identifié par SELEX des motifs de fixation optimale du dimère Nrd1-Nab3. Un second volet de ma thèse porte sur la caractérisation d’une nouvelle voie de terminaison de la transcription dépendante du facteur Rap1. Rap1 est important pour la structure des télomères et c’est aussi un facteur de transcription ciblant des centaines de promoteurs. Il active ou réprime l’initiation de la transcription notamment en recrutant des complexes de remodelage de la chromatine sur les promoteurs ciblés. De façon surprenante, le motif de fixation de ce facteur a été identifié dans des séquences capables de terminer la transcription isolées au laboratoire. Mes travaux ont permis de caractériser le mécanisme de terminaison par Rap1 et de distinguer cette voie des voies de terminaison canoniques. Ce facteur, lié à l’ADN, agit comme une barrière en bloquant la progression de l’ARN polymérase II par un mécanisme de « road-block ». Les polymérases ainsi arrêtées sont ciblées par une voie qui permet leur élimination lorsqu’elles sont bloquées par des dégâts sur l’ADN, impliquant leur ubiquitination et vraisemblablement leur dégradation par le protéasome. Les ARN libérés sont polyadénylés par la poly(A)-polymérase Trf4 et dégradés par l’exosome nucléaire. Ce mécanisme de terminaison est utilisé dans un contexte naturel puisque j’ai identifié des transcrits endogènes de S. cerevisiae terminés par cette voie. Nous proposons que la terminaison par Rap1 contribue au contrôle de la transcription envahissante. Ce facteur assurerait ainsi au niveau des promoteurs qu’il lie une double fonction de facteur de transcription et de protection de ces promoteurs contre l’interférence transcriptionnelleTranscription termination is essential, both for the 3’ end formation of functional transcripts and to avoid transcriptional interference between adjacent transcription units. This is particularly important in a compact genome such as S. cerevisiae. Termination is also one of the main strategies used by the cell to control and limit the “pervasive” or “hidden” transcription. In S. cerevisiae, RNA pol II is responsible for the transcription of the mRNAs and numerous non-coding RNA families such as the sn(o)RNAs and the CUTs (Cryptic Unstable Transcripts). CUTs represent a large fraction of the “pervasive” or “hidden” transcription. There are two canonical transcription termination pathways for this RNA polymerase. They involve the cleavage and polyadenylation complex (CPF-CF), in particular for the mRNAs termination, or the NNS complex for sn(o)RNAs and CUTs termination. During my thesis I studied two aspects or the transcription termination: 1) the motifs involved in the NNS complex recruitment on RNA and 2) the identification and the characterization of a new termination pathway by Rap1. CPF-CF and NNS complex are both recruited on the nascent transcript and on the RNA pol II. The NNS complex binds the RNA through its subunits Nrd1 and Nab3 which recognize specific motifs. Nonetheless, even if these motif sequences are now known, their presence does not elicit the certain identification of NNS dependent terminators. To clarify the NNS dependent terminator structure and the organization of the motifs bound by Nrd1 and Nab3 I looked for the sequences involved in a specific CUT termination doing a random mutagenesis experiment and I identified by SELEX the Nrd1-Nab3 dimer optimal binding motifs. A second part of my thesis concerns the characterization of a new transcription termination pathway dependent on the Rap1 factor. Rap1 is important for the telomere structure and it is also a transcription factor that targets hundred of promoters. It activates or represses transcription initiation recruiting chromatin remodeling complexes on the targeted promoters. Surprisingly, the Rap1 binding motifs have been identified among sequences eliciting termination isolated in the laboratory. My work has led to the characterization of the termination mechanism by Rap1 and distinguished this pathway from the two canonical pathways. This factor, bound to DNA, acts as a barrier blocking the RNA pol II progression by a road-block mechanism. These arrested polymerases are targeted by a pathway responsible for the elimination of RNA pol II blocked by DNA damages, implying their ubiquitination and probably their degradation by the proteasome. The released RNAs are polyadenylated by the poly(A) polymerase Trf4 and degraded by the nuclear exosome. This termination mechanism is used in a natural context since I identified S. cerevisiae endogenous transcripts terminated by this pathway. We propose that the Rap1 termination contributes to the pervasive transcription control. This factor could elicit, on its bound promoters, a double function of both transcription factor and protection of these promoters against transcriptional interference
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Burton, Elliot N. "Functional Consequences of mtDNA Methylation on Mitochondrial Transcription Factor Binding and Transcription Initiation." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4185.
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The role of cytosine modifications on nuclear transcription has been well characterized, but the function of DNA methylation in the mitochondrial genome has not been determined. Previous studies conducted by the Taylor laboratory have shown overexpression of the mitochondrial isoform of DNMT1 leads to strand-specific changes in gene expression. Here, we show that increased mtDNMT1 expression leads to an increase in the polycistronic transcript encoding the ND1 and Cox1 sequences. In order to understand the mechanistic basis of these changes, we investigated the effects of CpG methylation in the heavy strand promoter on transcription initiation and TFAM binding. Methylation was found to increase transcription initiation from HSP1 and result in larger TFAM:DNA complexes forming at lower protein concentrations. Our data suggest a functional role for cytosine methylation in the mitochondria, which we propose may have an effect on oxidative phosphorylation and cellular function.
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Eustis, Robyn Lynn. "The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation." PDXScholar, 2015. https://pdxscholar.library.pdx.edu/open_access_etds/2522.
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All sequenced archaeal genomes encode a general transcription factor, TFE, which is highly conserved and homologous to the alpha subunit of the eukaryotic transcription factor TFIIE. TFE functions to increase promoter opening efficiency during transcription initiation, although the mechanism for this is unclear. The N-terminus of TFE contains a common DNA binding motif, a winged helix. At the tip of this winged helix is a highly conserved region of aromatic amino acids that is close to DNA during initiation. TFE activation can compensate for mutations in another transcription factor, TFB2, which is homologous to TFIIB. P. furiosus encodes two paralogs of the eukaryotic RNA polymerase II transcription factor TFIIB: TFB1 and TFB2. TFB2 lacks a portion of the highly conserved N-terminus, and functions in transcription complexes at a lower efficiency than TFB1. It has been demonstrated that the presence of TFE is able to assist in transcription with TFB2 in vitro bringing its efficiency to almost TFB1 levels. Thus, TFB2 provides a unique opportunity to evaluate the function of the TFE winged helix in transcription. In this study the aromatic patch of the TFE winged helix was mutated to test its role in activation of TFB1 and TFB2-containing transcription complexes, because this aromatic patch is required for full TFE activity especially when NTP concentrations are low.
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Palagi, Alexandre. "Découverte et analyse d’inactivateurs de transcription chez la Drosophile agissant comme amplificateurs dans différents contextes cellulaires." Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4006.
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Un des enjeux majeurs de la biologie moderne est de comprendre les mécanismes complexes régissant l’expression de gènes d’un organisme en développement. Alors que les activateurs (enhancers) ont été abondamment étudiés et analysés, seul un relatif petit nombre de répresseurs (silencers) a été identifié à ce jour et restent jusqu’à présent assez mal compris. Un nombre non négligeable de CRMs jouent par ailleurs un double rôle à la fois d’amplificateurs et d’inactivateurs de transcription en fonction de l’état ou du type cellulaire dans lequel ils se trouvent, rajoutant un niveau supplémentaire de à la régulation génique dans différents types cellulaires et tissus. De façon surprenante, nous avons découvert que tous les éléments ayant une activité de répression transcriptionnelle que nous avons identifiés, s’avèrent aussi avoir une activité d’activation transcriptionnelle dans d’autres contextes cellulaires. Nos résultats remettent donc en question le paradigme de deux catégories distinctes de CRMs et suggèrent que des milliers, ou plus, d’éléments bifonctionnels restent à être découverts chez la Drosophile et potentiellement 104-105 chez l’humain. Le référencement et la caractérisation de ces éléments devraient s’avérer utiles, si ce n’est cruciaux, afin de comprendre la façon par laquelle ces motifs d’expression sont encodés au sein des génomes d'organismes métazoaires et donc éventuellement chez l’HommeA major challenge in biology is to understand how complex gene expression patterns in organismal development are encoded in the genome. While transcriptional enhancers have been studied extensively, few transcriptional silencers have been identified and they remain poorly understood. Here we used a novel strategy to screen hundreds of sequences for tissue-specific silencer activity in whole Drosophila embryos. Strikingly, 100% of the tested elements that we found to act as transcriptional silencers were also active enhancers in other cellular contexts. These elements were enriched in highly occupied target (HOT) region overlap (Roy et al., 2010) and specific transcription factor (TF) motif combinations. CRM bifunctionality complicates the understanding of how gene regulation is specified in the genome and how it is read out differently in different cell types. Our results challenge the common practice of treating elements with enhancer activity identified in one cell type as serving exclusively activating roles in the organism and suggest that thousands or more bifunctional CRMs remain to be discovered in Drosophila and perhaps 104-105 in human (Heintzman et al., 2009). Characterization of bifunctional elements should aid in investigations of how precise gene expression patterns are encoded in the genome
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Greberg, Maria Hellqvist. "Cloning and characterization of FREACs, human forkhead transcription factors." Göteborg : Dept. of Cell and Molecular Biology, Göteborg University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39751934.html.
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GHNEIM, NADA. "Relations entre les codes de l'oral et de l'écrit : Contraintes et ambiguïtés." Grenoble 3, 1997. http://www.theses.fr/1997GRE39023.
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Cette etude a pour objet l'etude des relations bidrectionnelles entre le code de l'ecrit et celui de l'oral. Le support de ce travail est une grammaire de transcription orthographique-phonetique toph (phonetisation), et sa grammaire inverse de transcription phonetique-orthographique phot (orthographisation). Le formalisme de la grammaire de phonetisation de toph a ete etendu pour permettre d'elargir son champ de couverture de la langue. Differents outils d'analyse logique des grammaires de phonetisation ont ete developpes pour tracer et modifier la grammaire afin d'assurer la coherence entre les regles. Des primitives d'analyse quantitative ont ete construites afin de valider l'adequation des grammaires aux corpus a partir desquels elles ont ete induites. Les problemes de l'inversion d'une grammaire toph en une grammaire d'orthographisation phot ont ete poses formellement dans le but d'une interpretation linguisitque de l'inversion des regles de phonetisation. Il est montre que des contextuelles, de nature similaire aux contraintes linguistiques qui ont ete introduites a la grammaire toph du francais, peuvent etre transcrites dans les processus d'orthographisation et qu'il est donc possible de limiter les solutions multiples homophoniques de l'orthographisation en empechant la production de solutions linguistiquement aberrantes. Enfin, ont ete mis au point une methode et des outils pour l'etude d'un corpus de mots deviants orthographiquement, le corpus orthotel. Les resultats de ce traitement, qui corroborent les typologies sociolinguistiques proposees dans la litterature permettent d'envisager plusieurs methodes de correction de l'orthographe basee sur des performances reelles de scripteurs humainsThe aim of this thesis is to study the bidrectionnal relations between the writing and the oral codes. The material is an orthographic-phonetic transcription grammar toph (letter-to-sound), and its inverse grammar of phonetic-orthographic transcription phot (sound-to-letter). The formalism of the grammar toph was extended in order to enlarge its field of coverage of the language. Different tools of toph grammars logical analysis were developed in order to trace and modify the grammar to insure the consistency between the rules. A quantitative analysis primitive was constructed in order to validate the grammars' adequacy to the corpora from which they were induced. The inversion of a toph grammar in a phot grammar arose problematics which were formally defined to give a linguistic interpretation of the inversion of the letter-to-sound rules. It is shown that contextual constraints similar in nature to the linguistic constraints and introduced to the french toph grammar, could be transliterated in phot grammar, and that it is therefore possible to limit the multiple homophonic solutions issued from this process, which prevent the production of linguistically aberrant solutions. Finally, was built a method and tools to study a corpus of orthographically deviant words, the orthotel corpus. The results of this treatment, which corroborate the socio-linguistical typology proposed in literature, allow to consider several spelling correction methods based on real human productions
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Apostolov, Apostol. "Studying the posttranslational modifications of transcription factor Ikaros and their role in its function." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00923158.
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The main topic of my PhD studies was to investigate the role of sumoylation in the function of Ikaros transcription factor, that regulates the lymphocyte differentiation and function. Sumoylation is a posttranslational modification that can change the properties and regulate the function of a given protein. Up to now, one study addressed the question of how sumoylationmodulates Ikaros function. It shows that Ikaros is sumoylated in total primary thymocytes, and that this dynamic event modulates Ikaros' repressive function. It also describes two consensus sumoylation sites on Ikaros (K58 and K240), the sumoylation of which leads to loss of Ikaros repressive function in ectopic reporter gene assays. The final conclusion of the study is that sumoylation does not alter the nuclear localization of Ikaros but acts as a mechanism disrupting its participation in both histone deacetylase (HDAC) dependent and independent repression. My work shows the presence of additional sumoylation site on Ikaros and demonstrates that sumoylation does not significantly alter its interaction with the nucleosome remodelling and histone deacetylase (NURD) complex in T-cell lines. The functional analysis of sumo-deficientmutants indicates a complex role of this modification in regulating Ikaros' transcriptional properties. The identification of this new sumoylation site contributes to a better understanding of Ikaros' dual repressive - activating function and suggests the existence of conditional Ikaros' interacting partners. Moreover, the different Ikaros splicing isoforms would have differentsumoylation profiles, which would complete the knowledge of their functional diversity.
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Liu, Xun. "Transcription-dependent and transcription-independent functions of the classical progesterone receptor in Xenopus ovaries." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26700.
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The physiological functions of the classical progesterone receptor (XPR) in regulating oocyte maturation and ovulation in Xenopus laevis remain controversial. Using antibodies generated against cloned XPR, I demonstrated here that the somatic follicle cells expressed an 80 kDa XPR protein, termed XPR-1. XPR-1 underwent progesterone-induced, proteasome-mediated degradation. A smaller (∼70 kDa) XPR protein, termed XPRo, was expressed in oocytes, but not in follicle cells. XPRo underwent progesterone-induced hyperphosphorylation, but not degradation. Treating isolated ovaries with progesterone caused oocyte maturation and the release of the mature oocytes from the ovaries (ovulation). Actinomycine D, a general transcription inhibitor, did not interfere with progesterone-induced oocyte maturation but blocked ovulation so that mature oocytes were trapped in the follicles. These results demonstrated that progesterone had dual functions in the process of ovulation: transcription-dependent follicle rupture and transcription-independent oocyte maturation. Furthermore, our results suggest that the dual functions of progesterone in Xenopus ovaries are mediated by the two forms of XPR proteins differentially expressed in the follicle cells and the oocytes respectively.
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Wu, Ming-Hsiao. "Temperature Dependent Transcription Initiation in Archaea: Interplay between Transcription Factor B and Promoter Sequence." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/2021.
Full textAbstract:
In Pyrococcus furiosus (Pfu), a hyperthermophile archaeon, two transcription factor Bs, TFB1 and TFB2 are encoded in the genomic DNA. TFB1 is the primary TFB in Pfu, and is homologous to transcription factor IIB (TFIIB) in eukaryotes. TFB2 is proposed to be a secondary TFB that is compared to TFB1, TFB2 lacks the conserved B-finger / B-reader / B-linker regions which assist RNA polymerase in transcription start site selection and promoter opening functions respectively. P. furiosus, like all Archaea, encodes a single transcription factor E (TFE), that is homologous to the N-terminus of transcription factor II E (TFIIE) α subunit in eukaryotes. TFE stabilizes the transcription bubble when present, although it is not required for in vitro transcription. In this study, in vitro transcription is used to reveal how TFB2 responds to different temperature (65 °C, 70 °C, 75 °C, 80 °C, and 85 °C) at promoters for three different kinds of gene: non-temperature responsive, heat-shock induced, and cold-shock induced in the absence or presence of TFE. The activity of transcription complexes formed by TFB2 is always lower than by TFB1 in all temperatures and promoters. However, with heat-shock gene promoters, the activity of transcription complexes formed by TFB2 increases more than those formed with TFB1 with increasing temperatures. The temperature-dependent activities of TFB1 and TFB2 are similar with the non-temperature responsive gene promoter. With the cold-shock gene promoter, the activity of transcription complexes formed by both TFB1 and TFB2 has the highest activity in lower temperatures. When TFE is present, the activity of transcription complexes formed by TFB2 is enhanced with heat-shock gene promoters particularly at lower temperatures, and makes TFB2 behave more similarly to TFB1. With the non-temperature responsive gene promoter, TFB2 still behaves similarly to TFB1 when TFE is present. However, with the cold-shock gene promoter, most of the activity of transcription complexes formed by TFB1 and TFB2 remain the same, but only the activity of TFB1 decreases at 75 °C. The results suggest that TFB2 may play a role in heat-shock response through its increased sensitivity to temperature, and that TFE can modulate this temperature response.