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Imada, Minatelli Sabrina Yuri [Verfasser], Uwe [Akademischer Betreuer] Groß, Uwe [Gutachter] Groß, Fabian Moritz [Gutachter] Commichau, and Wolfgang [Gutachter] Bohne. "Characterization of genes differentially regulated after bile acid exposure in Campylobacter jejuni / Sabrina Yuri Imada Minatelli ; Gutachter: Uwe Groß, Fabian Moritz Commichau, Wolfgang Bohne ; Betreuer: Uwe Groß." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2019. http://d-nb.info/1193728371/34.
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Watkinson, Jonathan I. "Characterization of two genes, trehalose-6-phosphate synthase/phosphatase and nucleotide binding protein, shown to be differentially regulated in roots of Cypripedium parviflorum var. pubescens grown with a mycorrhizal fungus Thanatephorus pennatus." Diss., Virginia Tech, 2002. http://hdl.handle.net/10919/27467.
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The analysis of gene changes associated with formation of the mycorrhizal symbiosis between orchid and fungi could have broad implications for plant pathogen interactions. Fungi associated with North American terrestrial orchids were once included in the pathogenic genus Rhizoctonia. This suggests that orchids are able to overcome or utilize normally pathogenic pathways to establish symbioses. A differential display technique was employed to analyze gene changes in orchid in response to a fungus. Samples of RNA from roots of Cypripedium parviflorum var. pubescens (CyPP) grown in the presence or absence of a mycorrhizal fungus; Thanatephorus pennatus, were analyzed using AFLP differential display. Forty-four fragments were selected out of 5000 as being differentially expressed, but only 15 sequences were obtained. Most showed homology to ribosomal genes. Two represented genes believed to be regulated by the mycorrhizal interaction: trehalose-6-phosphate synthase/phosphatase (Tps), which showed down-regulation and nucleotide binding protein (NuBP), which showed up-regulation. The Tps partial clone identifies 2100 bp at the 3' end of the gene and encodes a protein of 667 amino acids. The NuBP gene is approximately 1200bp in length and encodes a protein of 352 amino acids. The Tps gene exists in multiple copies with high expression in roots and low expression in rhizomes and leaves. The NuBP gene exists as a single copy and has a low level of expression in rhizomes and leaves. Expression of Tps is induced by sucrose, but reduced by trehalose. Cultivation of CyPP with non-mycorrhizal fungi did not affect expression of Tps or NuBP. Trehalose induced NuBP expression whereas sucrose did not. A second species of mycorrhizal fungi induced expression of NuBP but reduced expression of Tps. Analysis of Tps expression in Arabidopsis was done using promoter:GUS fusions. The Tps promoter:GUS plants revealed that Tps expression is constitutive in roots. Regulation of Tps driven GUS is expressed throughout seedlings. GUS was not detected in leaves of older plants but was detected in anthers and stigmatic surfaces of flowers. Expression of GUS driven by Tps showed a strong wound response and was present in the junction between siliques and pedicels.Ph. D.
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Ezer, Nadine. "Gene expression is differentially regulated in the epididymis after orchidectomy." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78357.
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The epididymis is the site for the transport, maturation and storage of spermatozoa. It is well established that epididymal structure and function are dependent on the testis for circulating androgens and factors in luminal fluid. Using cDNA microarrays, our objective is to characterize the expression of genes that are regulated over the first week post-orchidectomy in the epididymis of the adult Brown Norway rat. We describe four patterns of gene expression that are simultaneously activated in the epididymis after orchidectomy. We identify potential androgen-dependent genes including glutathione S-transferases and calcium-binding proteins, as well as potential androgen-repressed genes such as glutathione peroxidase-1. The expression of heat shock proteins, cyclins, and apoptosis-associated genes are described in the epididymis after orchidectomy. These results form the first comprehensive analysis of testis-regulated gene expression in the epididymis. This study is the first to demonstrate that gene expression is differentially regulated in the epididymis after orchidectomy.
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Daniels, Damon. "NF-κB-regulated differential gene transcription : a systems biology analysis." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/nfkappabregulated-differential-gene-transcription-a-systems-biology-analysis(f25d85c4-5463-4d41-bbb0-d23e6265fda8).html.
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The NF-κB transcription factor is expressed in the majority of mammalian cells and regulates a large number of genes with important functions in a variety of cellular processes including cell growth, division, apoptosis and inflammatory responses. Perturbation of NF-κB response has been implicated in a variety of diseases such as asthma and inflammatory bowel disease, in addition to various forms of cancer. Through experiments at the single cell level it has been shown that NF-κB displays complex temporal activation, notably including nucleo-cytoplasmic oscillations. It has been observed that these oscillations occur in a heterogeneous manner; as such they are masked when measured at the population level. In contrast, pulsed TNFα treatment at 100 min intervals produces regular and synchronous nuclear peaks of NF-κB. Such pulsatile stimulation may reflect more accurately physiological conditions. The work in this project uses a Systems Biology approach consisting of bioinformatic, mathematical, and experimental methodologies to investigate how NF-κB can regulate such a diverse set of gene responses. Previously published studies have proposed that target gene expression levels following NF-κB activation (continuous TNFα) can be explained by a combination of key parameters, including transcript degradation rate, transcript structure, and transcription initiation rate. Initial work in this project highlighted that these explanatory factors are not sufficient to describe the observed temporal order of gene transcription. The roles of miRNAs and NF-κB subunit phosphorylation in regulation were additionally explored. A large set of genes was identified that are activated more strongly by pulsed TNFα than by continuous TNFα treatment. This suggests a new unreported mechanism of gene regulation, the possible causes of which are examined in this thesis. The gene list was refined by altering pulse frequency, which revealed an enrichment of NF-κB targets correlated with the regularity of these pulses. Temperature shift and anti-inflammatory drug treatment (Diclofenac) were shown to have a profound effect on NF-κB oscillation frequency. These perturbations provide an alternative method to study the effects of NF-κB oscillation frequency on specific target genes, independent of a pulse regime. Integration and analysis of these datasets suggested that a core, frequency-encoded set of genes regulated by NF-κB might exist. It is proposed that such genes may respond optimally to specific frequencies of NF-κB activation, implying a potential frequency threshold. The presence of such genes may explain the need for the complex systems that control NF-κB timing. It was noted that there was an enrichment of genes encoding transcription factors within the frequency encoding set, in addition to proteins which are known to be involved in the control of inflammation.
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Styczynska-Soczka, Katarzyna. "Regulation and function of Rootletin, a gene differentially expressed in Drosophila sensory neurons." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15889.
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Drosophila melanogaster is a widely used and efficient genetic model to study nervous system development. The conservation of many genes from Drosophila to vertebrates and a short reproduction cycle makes the fruitfly a great tool for providing insight into crucial events in nervous system formation. In studying the development of the sensory nervous system, Drosophila also provides a model for understanding the formation and function of structurally diverse cilia. Cilia are hairlike organelles present throughout our bodies and responsible for many processes such as chemo, mechano, and thermosensation, fluid movement, hearing and fertility. In Drosophila the only somatic ciliated cells are the Type I sensory neurons in which a cilium forms the sensory dendrite. There are more than two diverse subtypes of the ciliated sensory neurons and the mechanism by which this diversity is achieved remains unclear. The mechanism of ciliated sensory neuron differentiation was hereby studied on an example of a differentially expressed ciliary gene - CG6129 - a Drosophila orthologue of human Rootletin, a main protein components of ciliary rootlets. CG6129 expression is specific to the ciliated cells and exhibits so called chordotonal-enriched pattern - a strong and permanent expression in the chordotonal subtype of type I neurons and weaker and transient expression in the external sensory subtype. I have shown that CG6129 knock-down causes severe disruption of the chordotonal organs function without any obvious change in the structure of the cilium, other than the lack of ciliary rootlet. The function of the external sensory subtype was only slightly affected which further highlights the difference between the two types of ciliated sensory organs. The fact that CG6129 is differentially expressed in the two subtypes of the Drosophila ciliated sensory neurons suggests that the genes involved in the formation of various cilia are differentially regulated. I have shown that CG6129 is regulated by the two well known ciliary transcription factors - RFX and fd3F (distant homologue of Foxj1). Of the two enhancers found the early-to-late enhancer is almost entirely dependent on RFX and not on fd3F while the late enhancer is dependent on both fd3F and RFX. The fact that there is some residual CG6129 expression in the absence of both RFX and fd3F suggests involvement of another regulator that may contribute to the cilia diversity. Zmynd10 is a recently characterised ciliary gene that is involved in the axonemal dynein arms assembly. Mutations in human Zmynd10 cause primary ciliary dyskinesia (PCD) and Drosophila Zmynd10 mutants have immotile cilia that lack dynein arms. Due to the presence of specific protein domains Zmynd10 has been suggested to act as a transcriptional regulator. I have shown that the transcript levels of CG6129 and other ciliary genes are reduced in the Zmynd10 mutant. This implies that Zmynd10 may regulate ciliary genes on a transcriptional or post transcriptional level and may contribute to the regulatory network governing ciliogenesis.
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Tsourdi, Elena, Juliane Salbach-Hirsch, Martina Rauner, Tilman D. Rachner, Stephanie Möller, Matthias Schnabelrauch, Dieter Scharnweber, and Lorenz C. Hofbauer. "Glycosaminoglycans and their sulfate derivatives differentially regulate the viability and gene expression of osteocyte-like cell lines." Sage, 2014. https://tud.qucosa.de/id/qucosa%3A35689.
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Collagen and glycosaminoglycans, such as hyaluronan and chondroitin sulfate, are the major components of bone extracellular matrix, and extracellular matrix composites are being evaluated for a wide range of clinical applications. The molecular and cellular effects of native and sulfatemodified glycosaminoglycans on osteocytes were investigated as critical regulators of bone remodeling. The effects of glycosaminoglycans on viability, necrosis, apoptosis, and regulation of gene expression were tested in two osteocyte-like cell lines, the murine MLO-Y4 and the rat UMR 106-01 cells. Glycosaminoglycans were non-toxic and incorporated by osteocytic cells. In MLO-Y4 cells, sulfation of glycosaminoglycans led to a significant inhibition of osteocyte apoptosis, 42% inhibition for highly sulfated chondroitin sulfate and 58% for highly sulfated hyaluronan, respectively. Cell proliferation was not affected. While treatment with highly sulfated chondroitin sulfate increased cell viability by 20% compared to the native chondroitin sulfate. In UMR 106- 01 cells, treatment with highly sulfated hyaluronan reduced the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio by 58% compared to the non-sulfated form, whereas highly sulfated chondroitin sulfate led to 60% reduction in the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio in comparison to the native chondroitin sulfate. The expression of SOST, the gene encoding sclerostin, was reduced by 50% and 45% by highly sulfated hyaluronan and chondroitin sulfate, respectively, compared to their native forms. The expression of BMP- 2, a marker of osteoblast differentiation, was doubled after treatment with the highly sulfated hyaluronan in comparison to its native form. In conclusion, highly sulfated glycosaminoglycans inhibit osteocyte apoptosis in vitro and promote an osteoblast-supporting gene expression profile.
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Williamson, William Iain. "Differential chromatin topology and transcription factor enhancer binding regulate spatiotemporal gene expression in limb development." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8056.
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Many developmental genes are located in gene-poor genomic regions and are activated by long-range enhancers located up to 1Mb away. Modification and reorganisation of chromatin structure is pivotal to such long-range gene regulation. A prerequisite for enhancer activity is the binding of transcription factors and co-factors with the interplay between activating and repressive factors determining tissue, spatial and temporal specificity. Spatiotemporal control of sonic hedgehog (Shh) and the 5′ Hoxd genes (especially Hoxd13) is crucial for vertebrate limb anterior-posterior (A-P) axis and autopod patterning. Shh tissue specificity is controlled by multiple enhancers throughout an adjacent gene desert. The ~0.8Mb-distant limb enhancer (ZRS) bypasses nearby genes to activate only Shh. In contrast, limb-specific HoxD expression is regulated by multiple enhancers, with the ~200kb-distant global control region (GCR) regulatory element the most characterised. In this thesis I investigated the mechanisms of ZRS and GCR regulation of Shh and Hoxd13 respectively. The model system used was immortalised cell lines derived from the anterior and posterior distal forelimb buds of E10.5 and E11.5 mouse embryos. Cell line data were confirmed in dissected limb tissue. Increased expression of the 5′ Hoxd genes, particularly Hoxd13, correlated with the loss of the repressive, polycomb catalysed, histone modification H3K27me3 and decompaction of chromatin structure over the HoxD locus at the distal posterior forelimb bud at stage E10.5. Moreover, I show that the GCR spatially co-localises with the 5′ HoxD locus at the distal posterior region of E10.5-11 embryos. These data are consistent with the formation of a chromatin loop between Hoxd13 and the GCR at the time and place of distal limb bud development when the GCR is required to initiate 5′ Hoxd gene expression. This is the first example of A-P differences in chromatin compaction and local folding in the limb. Point mutations within the ZRS cause ectopic (anterior) Shh expression, which results in preaxial polydactyly (PPD). The ZRS contains multiple canonical ETS transcription factor binding motifs, and point mutations in two families with PPD results in the formation of additional ETS binding sites. The point mutations cause the loss or reduction of ETV4/5 transcription factor binding at a non-canonical ETS binding site and enable additional binding instead of ETS1. I show that ETV4/5, ETS1 and another ETS protein GABPα all bind to the ZRS. This work has revealed the differential effect on Shh expression of two groups of ETS factors mediated through the ZRS. The binding of ETS1/ GABPα determines the posterior Shh expression domain while ETV4/5 restricts anterior Shh expression. Two point mutations alter the ETS-binding profile, creating an additional ETS1/ GABPα site that is sufficient to drive ectopic Shh expression. DNA FISH on E11.5 forelimb and floorplate tissue sections revealed that the Shh-ZRS genomic locus is in a compact chromatin conformation in both Shhexpressing and non-expressing cells. However, I show that the ZRS co-localises with Shh to a significantly greater extent in the distal posterior limb bud and the floorplate compared with cells where Shh is not expressed. This thesis presents novel research into long-range gene regulation during limb development, elucidating the role of chromatin re-organisation and how spatial-specific enhancer activity is determined by opposing sets of binding factors.
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Emilsson, Lina. "Detection of Differentially Expressed Genes in Alzheimer's Disease : Regulator of G-protein Signalling 4: A Novel Mediator of APP Processing." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5910.
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Mai, Hans-Jörg [Verfasser], and Petra [Akademischer Betreuer] Bauer. "Analysis of differential protein and gene expression in Arabidopsis thaliana depending on iron supply and the abundance of the central iron uptake regulator FIT (Fer-like Iron Deficiency-induced Transcription Factor) and investigations on possible post-translational modifications of FIT / Hans-Jörg Mai. Betreuer: Petra Bauer." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2014. http://d-nb.info/1109790228/34.
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Romero, barrios Natali. "Non-codings RNAs, regulators of gene expression in Arabidopsis thaliana root developmental plasticity Noncoding Transcription by Alternative RNA Polymerases Dynamically Regulates an Auxin-Driven Chromatin Loop Battles and hijacks: noncoding transcription in plants Long noncoding RNA modulates alternative splicing regulators in Arabidopsis Detection of generic differential RNA processing events from RNA-seq data." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS128.
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Les techniques de séquençage à haut-débit développées ces dernières années ont permis d'identifier des milliers d’ARN non-codants et des événements tels que l’épissage ou l’édition. Cette approche est à l’origine d’une meilleure compréhension des mécanismes régulant l'expression des gènes. Les longs ARN non-codants (lncARN) ont ainsi émergé comme des acteurs clés de la régulation de divers processus développementaux. Ils agissent soit directement sous leur forme longue par des interactions lncARN-protéine(s) soit après une étape de maturation qui génère des siARN ou des miARN régulateurs, menant à l’extinction génique par clivage des ARNm, la répression de la traduction ou en entrainant des modifications épigénétiques (ADN/chromatine) de leurs cibles. L’objectif de cette thèse était d’élucider les mécanismes d'action de lncARNs dans le développement de la plante. J'ai contribué à l'analyse de l'action du lncARN APOLO dans la régulation de la topologie de la chromatine chez Arabidopsis thaliana. Ensuite, j’ai concentré mes efforts sur le lncARN ASCO (Alternative Splicing COmpetitor) qui interagit avec les protéines NSRs (Nuclear Speckles RNA-binding Proteins) et participent au patron d’épissage de certains gènes cibles. Lors d’un traitement par l’auxine, NSRb est induit alors qu’ASCO est réprimé dans les racines. Le même type de traitement, chez le double mutant nsra/b et les lignées surexprimant ASCO, entraine déficience partielle dans la formation des racines latérales. En utilisant un nouvel outil bio-informatique appelé "RNAprof", nous avons détecté 1885 ARN différentiellement maturés entre le mutant nsra/b et la lignée sauvage traités à l’auxine. Parmi ces gènes, nous avons identifié ARF19, un régulateur clé de la voie de signalisation de l’auxine au cours de l'initiation et le développement de la racine. J’ai démontré qu'ARF19 interagit directement avec les NSRs et qu’il est différentiellement polyadénylé dans le double mutant nsra/b, conduisant à une isoforme plus courte du transcrit ARF19. D’autre part, parmi les gènes dérégulés de manière transcriptionnelle chez le mutant des gènes impliqués dans la signalisation par l’éthylène ont été identifiés. J’ai ensuite montré que plusieurs de ces gènes sont aussi dérégulés dans les plantes mutantes arf19-1 et arf19-2 en réponse à l’auxine, soutenant un rôle d'ARF19 dans la réponse croisée entre l’auxine et l’éthylène. Le gène NSRb est induit par l'éthylène et l'inhibition de la synthèse d'éthylène par l'AVG complémente le phénotype de racine latérale du mutant nsra/b en réponse à l’auxine. De plus, l'AVG et la surexpression d’ASCO augmentent l'accumulation de l’isoforme courte d’ARF19. Cette étude met en avant la capacité du lncARN ASCO à moduler l’épissage par le détournement des NSRs et la capacité des ARN non-codants à moduler l’épissageIn the last years, high-throughput sequencing techniques have made possible to identify thousands of noncoding RNAs and a plethora of different mRNA processing events occurring in higher organisms. This led to a better understanding of different regulatory mechanisms controlling gene expression. Long noncoding RNAs (lncRNAs) are emerging as key players in the regulation of varied developmental processes. They can act directly in a long form by lncRNA-protein interactions or be processed into shorter small si/miRNAs, leading to mRNA cleavage, translational repression or epigenetic DNA/chromatin modification of their targets. In this study, we aim to understand the mechanism of action of lncRNAs in plant development. Initially, I contributed to the analysis of the action of the APOLO lncRNA in chromatin topology regulation. Then, I focused my work on the lncRNA ASCO (Alternative Splicing COmpetitor) that interacts with NSRs (Nuclear Speckles RNA-binding Proteins) to modulate the splicing pattern of NSR-regulated mRNA targets. Auxin treatment induces NSRb and represses ASCO expression in roots. The nsra/b double mutant and ASCO overexpressing lines treated with auxin are partially impaired in lateral root formation. Using a new bioinformatic tool called “RNAprof”, we detected 1885 differential RNA processing events genome-wide in auxin-treated nsra/b mutants compared to WT. Among them, we identified ARF19, a key regulator of auxin signaling in lateral root initiation and development. I demonstrated that ARF19 is directly bound by both NSRs and that in the nsra/b double mutant ARF19 is alternatively polyadenylated leading to a short transcript isoform. Furthermore, among the transcriptionally deregulated genes in the nsra/b mutant plants, I identified an important group related to ethylene response. I further showed that several of these genes are also deregulated in the arf19-1 and arf19-2 mutants plants in response to auxin, supporting a role of ARF19 in the auxin-ethylene crosstalk. NSRb is also induced by ethylene and the inhibition of ethylene synthesis by AVG rescues the nsra/b double mutant lateral root phenotype in response to auxin. Moreover, AVG and ASCO overexpression lead to increased accumulation of the ARF19 short isoform. Altogether, this study shed new light on the role of the lncRNA ASCO in the regulation of RNA processing by hijacking NSRs and the capacity of non-coding RNAs to modulate splicing
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Imada, Minatelli Sabrina Yuri. "Characterization of genes differentially regulated after bile acid exposure in Campylobacter jejuni." Doctoral thesis, 2019. http://hdl.handle.net/21.11130/00-1735-0000-0003-C19D-2.
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GUPTA, ABHISHEK. "INDENTIFICATION OF DIFFERENTIALLY REGULATED GENES BETWEEN NORMAL AND TNF INDUCED IN HUMAN TRANSCRIPTOME." Thesis, 2021. http://dspace.dtu.ac.in:8080/jspui/handle/repository/19588.
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According to Human Genome Project humans contains nearly 25,000 genes. Humans differs
from each other just because of 0.1% of DNA. Since all the cells of an individual contains
similar genetic material still they differ among one another in function and this is because of
the differential gene expression. Since cells respond differently to different stimulus it is
interesting to note their response. Gene expression is the main reason how cell gone a respond
to different stimuli. In this study we have taken sequenced mRNA from human cell lines which
was treated with TNF-alpha for some time period and try to identify all the differential
expressed genes using RNA-Seq. We will extend our study to find out the pathways in which
these genes have involved.
In this study we have used DESeq2 package for normalization, statistical analysis and for
visualization of dataset. Genes obtained at the end of the analysis can be act as biomarkers for
the cancer treatment.
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Chen, Wuu-Yang, and 陳武揚. "Characterization of Catharanthus roseus Genes Regulated Differentially by Peanut Witches'' Broom Phytoplasma Infection." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/78285063901289446129.
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博士國立臺灣大學
植物病理與微生物學研究所
99
The differential display (DD) strategy was applied to isolate periwinkle (Catharanthus roseus) cDNAs differentially expressed following infection with peanut witches'' broom (PnWB) phytoplasma. Sixty four clones have been selected from differentially expressed cDNA fragments. After screening by reverse northern hybridization, 10 transcripts were selected and sequenced. The expression levels of them was quantified by real-time polymerase chain reaction (PCR), and 7 DD transcripts were identified as ones truly differentially expressed after PnWB phytoplasma infection. One showing homology with phi-1 gene was up-regulated, while the others were down-regulated. Except two of which were predicted protein genes, the other down-regulated genes share homology with psaDa gene, ML domain protein gene, eukaryotic translation initiation factor SUI1 gene, and plastidic aldolase NPALDP1 gene. Homologous genes were further confirmed for 3 DD transcripts by isolating full-length cDNA fragments from the cDNA library constructed in this study. Confirmed genes included ML domain protein gene, translation initiation factor SUI1 gene, and plastidic aldolase NPALDP1 gene, and were mainly involved in innate immune responses, stress responses, and photosynthesis. In the time course experiments, expression levels of these three genes were down-regulated at 6th week after inoculation, and the results agreed with those of differential display. The possible role of these genes in the periwinkle that was infected by PnWB phytoplasma is discussed.
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Chen, Yu-Hsiang, and 陳祐祥. "The identification of litter size related single nucleotide polymorphisms from differentially regulated genes of early embryo in Landrace sows." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/48284270286676623701.
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碩士國立臺灣大學
動物科學技術學研究所
96
Reproductive traits, especially litter size, are important components for reducing the costs of pig production. DNA molecular markers can be used for marker-assisted selection (MAS) program through candidate gene approach to improve the rate of selection response. Landrace is the major strain of sow used in commercial pig production in Taiwan but there is no available molecular marker associated with purebred Landrace. The survival and proper development of early embryos are important factors affecting the reproductive traits of sows. The purpose of this study is to discover the SNPs located on the regulatory regions of differentially expressed genes between morula and blastocyst. We also characterized the SNP genotypes of these genes and studied the association of litter size with these genotypes in Landrace sows. After cloning and sequencing regulatory region of the 10 candidate genes in 30 Landrace sows, we found 59 novel SNPs. Furthermore, we genotyped the SNP markers within the candidate genes in 161 Landrace sows. The effects of SNP markers on total number of pigs born (TNB) and number born alive (NBA) were tested. Our results showed the SNPs located on ataxia-telangiectasia mutated (ATM) gene, plasma platelet-activating factor acetylhydrolase (plasma PAFAH) gene and prolactin (PRL) gene were associated with TNB and NBA (P < 0.05). As most of these SNPs located on the regulatory sequences of the candidate genes, they may have direct effects on regulating expression levels of those genes. We therefore propose ATM, plasma PAFAH and prolactin, the host genes for litter size related SNPs, are likely to have major effects on litter size in pigs, and these efforts may help us to improve the reproductive efficiency of pigs. We developed an efficient and effective platform based on litter size related SNPs associated with the regulatory sequences of differentially regulated genes from morula to blastocyst preimplantation embryos. Once validated further with larger sample size from multiple farms, this SNP based screening platform will significantly facilitate the selection of best breeding herd of Landrace sow.
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García, Palma Lizet Elena [Verfasser]. "Microarray analysis of differentially regulated genes in human leukemia cells after expression of the inositol 5-phosphatase SHIP / vorgelegt von Lizet Elena García Palma." 2006. http://d-nb.info/980226368/34.
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Jan, Fei Wen, and 詹斐雯. "Differential expression of HIF-1α regulated genes in OSCC cells in response to abrasion." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/awtzby.
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Jen-LingWang and 王仁伶. "Novel Genes that Are Regulated by NRF-1 and Have Differential Functions in Neurite Outgrowth." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/26800864057545539240.
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博士國立成功大學
基礎醫學研究所
101
Nuclear respiratory factor-1 (NRF-1) is a major transcription factor in the human genome and plays a key role in neurite outgrowth in human neuroblastoma IMR-32 cells. Neurite outgrowth is a critical process in neuronal development, and many genes are involved in this well-regulated process. However, how NRF-1 regulates neurite outgrowth is still unclear. In this study, we used bioinformatic tools to search for genes downstream from NRF-1 and hypothesized that these genes mediate NRF-1 function in neurite outgrowth in neurons. In the first part of this study, we hypothesized that synapsin I is downstream of NRF-1 and mediates its function in neurite outgrowth. Synapsin I protein is a well-known phosphoprotein in neuronal terminals and has been implicated in neuronal differentiation. Human synapsin I gene promoter has a putative NRF-1 response element (NRE), but it is not known whether this NRE is functional. Gel electrophoretic mobility shift assays (EMSA), chromatin immunoprecipitation (ChIP), site-directed mutagenesis, and promoter studies indicated that NRF-1 is a positive regulator of synapsin I promoter. Exogenous NRF-1 overexpression increased synapsin I protein levels in IMR-32 and HEK293T cells. Down-regulating synapsin I expression markedly decreased the percentage of neurite-bearing cells and the average length of the longest neurites in IMR-32 cells that stably or transiently overexpressed NRF-1. We confirmed that the human synapsin I gene is positively regulated by NRF-1 and mediates the function of NRF-1 in neurite outgrowth. In the second part, genome-wide analyses have identified that 916 genes in the human genome are potential NRF-1-regulated genes, including 691 annotated and 225 hypothetical genes. Fifteen annotated genes from different biological processes, cell cycle-related genes- MAPRE3, NPDC1, SUV39H2, SKA3, transport-related genes- RAB3IP, TRAPPC3, signal transduction-related genes- SMAD5, PIP5K1A, USP10, SPRY4, transcription-related genes- GTF2F2, NR1D1, and regulation of GTPase activity-related genes- RHOA, RAPGEF6, SMAP1, were selected for biological confirmation. EMSA and ChIP confirmed that all NREs of these fifteen genes are critical for NRF-1 binding. Quantitative RT-PCR demonstrated that mRNA levels of 12 of these genes are regulated by NRF-1. Overexpression or knockdown of candidate genes demonstrated that MAPRE3, NPDC1, SMAD5, USP10, SPRY4, GTF2F2, SKA3, RAPGEF6 positively regulated, and RHOA and SMAP1 negatively regulated neurite outgrowth. In this part, we have confirmed that 12 annotated genes are regulated by NRF-1 and 10 of them mediate NRF-1 function in neurite outgrowth in IMR-32 cells. In the third part, we focused on three hypothetical genes, FAM134C, C3orf10, and ENOX1, and determine whether these hypothetical genes mediate NRF-1 function in neurite outgrowth in IMR-32 cells and primary hippocampal neurons. We found that NRF-1 positively regulated FAM134C and ENOX1, but negatively regulated C3orf10 in IMR-32 cells and primary rat cortical neurons. FAM134C positively regulates and C3orf10 negatively regulates neurite outgrowth, but ENOX1 plays no role in neurite outgrowth regulation. FAM134C and C3orf10 mediates NRF-1-enhanced neurite outgrowth. In primary rat hippocampal neurons, Fam134c is predominantly expressed in the axon hillock and C3orf10 is ubiquitously expressed in all neurites and cell bodies at different developmental stages, suggesting their roles in axonal and dendritic outgrowth. Fam134c positively regulates axonal length, but C3orf10 negatively regulates the number of axonal collaterals and dendrites. In the third part, we annotated FAM134C, C3orf10, and ENOX1 as NRF-1-regulated genes, which have differential effects on neurite outgrowth in neuroblastoma cells as well as neurons. Overall, we found that NRF-1 regulates neurite outgrowth through cell cycle-, transport-, signal transduction-, transcription-, regulation of GTPase activity-related genes and hypothetical genes, which suggest that NRF-1 regulates neuronal differentiation through a variety of biological processes. Keywords: nuclear respiratory factor-1; neuroblastoma cells; primary hippocampal neurons; neurite outgrowth; axonal and dendritic outgrowth; bioinformatics.
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Sun, Kuo-Lun, and 孫國倫. "High Salt Diet Differentially Regulated Pro-inflammatory Gene Expression in Renal Cortex of Spontaneously Hypertensive Rats." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/52784169963970759943.
Full textAbstract:
碩士長庚大學
基礎醫學研究所
92
High salt diet exacerbates hypertension in Spontaneously Hypertensive Rats (SHR), which is associated with structural changes and damages in the kidney. Since kidney plays an important role in initiating and maintaining hypertension, renal gene expression profile in response to high salt diet may reveal important factors associated with salt-sensitive hypertension that were previously overlooked. For this purpose, we employed oligonucleotide expression arrays (Agilent) to analyze gene expression profile in the renal cortex of SHR fed a high salt (8% NaCl) vs. normal salt (1% NaCl) diet for 3 wks. In this model, significant increase in systolic blood pressure (SBP) was observed 2 wks after initiation of high salt diet. At the third wk, SBP was 240 ± 4 and 219 ± 3 mmHg in rats with high vs. normal salt diet (p<0.05, n=8); whereas urinary volume, [Na+] and [Cl-] increased by 6.9, 4.3 and 3.7 fold, respectively. Hemodynamic study indicated that angiotensin II (50 ng/kg)-induced decrease in renal blood flow and increase in renal vascular resistance were enhanced by both 1-wk- and 3-wk-treatment with high salt diet (p<0.05, n=4-5), which was consistent with previous finding that high salt diet enhanced expression of AT1 receptor. Renal cortical mRNA from 3 rats in each group was pooled and subjected to analysis with rat oligonucleotide expression array and further verified by real-time polymerase chain reaction. The results reveal alterations of expression of some pro-inflammatory genes in the renal cortex of rat during the early stage of the development of salt-sensitive hypertension.
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Sprod, OR. "Differential expression of the GMCSF gene in the immune system regulated by epigenetic factors." Thesis, 2011. https://eprints.utas.edu.au/12957/1/Sprod_front.pdf.
Full textAbstract:
Granulocyte-macrophage colony stimulating factor (GM-CSF) is a cytokine that
stimulates the production of leukocytes as part of an immune response. The role that
GM-CSF plays in the immune system is reliant on its tightly controlled expression,
both temporally and spatially. The overall aim of this thesis was to investigate the
factors that contribute to the correct temporal and spatial expression of GM-CSF in
immune cells.
It was found that while GM-CSF expression can be stimulated in murine T cells but
not B cells, key transcription factors involved in GM-CSF gene expression were
present in both cell types, leading to the hypothesis that epigenetic mechanisms
underlie this differential response. In support of this, differences in DNA
methylation, histone modifications and the presence of chromatin remodelling
proteins were detected at the GM-CSF promoter between the two cell types.
DNA methylation levels were higher at a CpG dinucleotide in the GM-CSF promoter
in T compared to B cell lines, and DNA methylation of the GM-CSF promoter
blocked expression from a reporter plasmid. Demethylation of the promoter was not
sufficient to enable GM-CSF gene expression in B cells, although it increased its
expression in T cells. The effect of removing the CpG dinucleotide, which is
contained in an Sp1 transcription factor binding site, was also examined. In a
transiently transfected reporter model, removal of the Sp1 site resulted in loss of promoter activity. However, in a stably integrated transgene model, the Sp1 mutant
promoter exhibited an increased response to stimulation. The differential response of
the promoter mutant between the transient and stably transfected models suggests
that the chromatin environment of the gene plays an important role in transcriptional
regulation.
To further examine the importance of chromatin in GM-CSF gene regulation, histone
modifications were examined at the GM-CSF promoter in T and B cell lines. Several
key differences were observed. In T cells, acetylation of histone H3 was increased at
the GM-CSF promoter relative to B cells. Increasing promoter acetylation levels by
treatment with the histone deacetylase inhibitor Trichostatin A (TSA) facilitated
expression of GM-CSF in the B cell lines in response to stimulation. Furthermore,
TSA treatment in combination with DNA demethylation had a synergistic effect on
GM-CSF expression in both T and B cells. In contrast to histone acetylation, histone
H3 lysine 27 trimethylation was lower at the GM-CSF promoter in T cells relative to
B cells. Finally, the chromatin remodelling protein Brg1, which is known to interact
with acetylated histones, was present at the GM-CSF promoter in T cells at higher
levels than in B cells.
These data suggest that enrichment of histone H3 acetylation and Brg1 and decreased
H3K27Me3 contribute to the establishment of a ‘permissive’ chromatin environment
at the GM-CSF promoter in T cells, which is not present at the promoter in B cells.
A ‘permissive’ chromatin environment can be established at the GM-CSF promoter in B cells following treatment with TSA, which increases histone acetylation. This
allows remodelling of the promoter chromatin and subsequent gene expression in
response to immune signals. However, this induced ‘permissive’ state is not
maintained. Following removal of the inducing stimulus in A20 B cells, the
chromatin is reset to its original ‘repressive’ state and the GM-CSF gene becomes
unresponsive to subsequent stimulation.
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Aydin, Son Yeşim. "Differential expression of skin cancer and hair-follicle cycle regulated genes in tumor susceptible K14-Agouti mice." 2006. http://etd.utk.edu/2006/AydinSonYesim.pdf.
Full textAbstract:
Thesis (Ph. D.) -- University of Tennessee, Knoxville, 2006.Title from title page screen (viewed on September 14, 2006). Thesis advisor: Edward J. Michaud. Vita. Includes bibliographical references.
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Young, Sara Kathryn. "Upstream open reading frames differentially regulate genespecific translation in the integrated stress response." Diss., 2016. http://hdl.handle.net/1805/10606.
Full textAbstract:
Indiana University-Purdue University Indianapolis (IUPUI)Gene expression is a highly coordinated process that relies upon appropriate regulation of translation for protein homeostasis. Regulation of protein synthesis largely occurs at the initiation step in which the translational start site is selected by ribosomes and associated initiating factors. In addition to the coding sequences (CDS) for protein products, short upstream open reading frames (uORFs) located in the 5’-leader of mRNAs are selected for translation initiation. While uORFs are largely considered to be inhibitory to translation at the downstream CDS, uORFs can also promote initiation of CDS translation in response to environmental stresses. Multiple transcripts associated with stress adaptation are preferentially translated through uORF-mediated mechanisms during activation of the Integrated Stress Response (ISR). In the ISR, phosphorylation of α subunit of the translation initiation factor eIF2α (eIF2α~P) during environmental stresses results in a global reduction in protein synthesis that functions to conserve energy and nutrient resources and facilitate reprogramming of gene expression. Many key regulators of the ISR network are subject to preferential translation in the response to eIF2α-P. These preferentially translated genes include the pro-apoptotic transcriptional activator Chop that modifies gene expression programs, feedback regulator Gadd34 that targets the catalytic subunit of protein phosphatase 1 to dephosphorylate eIF2α~P, and glutamyl-prolyl tRNA synthetase Eprs that increases the charged tRNA pool and primes the cell for resumption of protein synthesis after stress remediation. Ribosome bypass of at least one inhibitory uORF is a common theme between Chop, Gadd34, and Eprs, which allows for their regulated expression in response to cellular stress. However, different features encoded within the uORFs of the Chop, Gadd34, and Eprs mRNAs provide for regulation of their inhibitory functions, illustrating the complexities of uORF-mediated regulation of gene-specific translation. Importantly, preferentially translated ISR targets can also be transcriptionally regulated in response to cellular stress and misregulation of transcriptional or translational expression of Gadd34 can elicit maladaptive cell responses that contribute to disease. These mechanisms of translation control are conserved throughout species, emphasizing the importance of translation control in appropriate gene expression and the maintenance of protein homeostasis and health in diverse cellular conditions.
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Singh, Suman K., Waqas A. Abbas, and Desmond J. Tobin. "Bone morphogenetic proteins differentially regulate pigmentation in human skin cells." 2012. http://hdl.handle.net/10454/6194.
Full textAbstract:
Bone morphogenetic proteins (BMPs) are a large family of multi-functional secreted signalling molecules. Previously BMP2/4 were shown to inhibit skin pigmentation by downregulating tyrosinase expression and activity in epidermal melanocytes. However, a possible role for other BMP family members and their antagonists in melanogenesis has not yet been explored. In this study we show that BMP4 and BMP6, from two different BMP subclasses, and their antagonists noggin and sclerostin were variably expressed in melanocytes and keratinocytes in human skin. We further examined their involvement in melanogenesis and melanin transfer using fully matched primary cultures of adult human melanocytes and keratinocytes. BMP6 markedly stimulated melanogenesis by upregulating tyrosinase expression and activity, and also stimulated the formation of filopodia and Myosin-X expression in melanocytes, which was associated with increased melanosome transfer from melanocytes to keratinocytes. BMP4, by contrast, inhibited melanin synthesis and transfer to below baseline levels. These findings were confirmed using siRNA knockdown of BMP receptors BMPR1A/1B or of Myosin-X, as well as by incubating cells with the antagonists noggin and sclerostin. While BMP6 was found to use the p38MAPK pathway to regulate melanogenesis in human melanocytes independently of the Smad pathway, p38MAPK, PI3-K and Smad pathways were all involved in BMP6-mediated melanin transfer. This suggests that pigment formation may be regulated independently of pigment transfer. These data reveal a complex involvement of regulation of different members of the BMP family, their antagonists and inhibitory Smads, in melanocytes behaviour.
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Stryjecki, Carolina. "Saturated and monounsaturated fatty acids differentially regulate adipokine gene expression and are associated with systemic C-Reactive Protein levels." Thesis, 2011. http://hdl.handle.net/10214/2990.
Full textAbstract:
This thesis investigates the contributions of fatty acids (FA) to adipokine dysregulation and inflammation. Differentiated 3T3-L1 adipocytes were treated with palmitic, stearic, palmitoleic, and oleic acids and changes in adipokine gene expression were measured. Here it was determined that saturated FA (SFA) increased the expression of RANTES and monounsaturated FA (MUFA) decreased the expression of RANTES and IL-6; demonstrating that FA differentially regulate adipokine expression. Relationships between plasma levels of SFA, MUFA and C-reactive protein (CRP) were also identified in a human observational study, further demonstrating the link between FA and inflammation Moreover, an association was also found between stearoyl-CoA desaturase 1 (SCD1) activity and CRP, demonstrating that SCD1 activity contributes to the inflammatory state. Genetic variation in SCD1 was also found to alter plasma FA and CRP levels, thus contributing to systemic inflammation. Taken together, these results demonstrate that SFA and MUFA influence adipokine dysregulation and systemic inflammation.
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Mardaryev, Andrei N., N. Meier, Krzysztof Poterlowicz, A. A. Sharov, T. Y. Sharova, Mohammed I. Ahmed, Valentina Rapisarda, et al. "Lhx2 differentially regulates Sox9, Tcf4 and Lgr5 in hair follicle stem cells to promote epidermal regeneration after injury." 2011. http://hdl.handle.net/10454/6079.
Full textAbstract:
The Lhx2 transcription factor plays essential roles in morphogenesis and patterning of ectodermal derivatives as well as in controlling stem cell activity. Here, we show that during murine skin morphogenesis, Lhx2 is expressed in the hair follicle (HF) buds, whereas in postnatal telogen HFs Lhx2(+) cells reside in the stem cell-enriched epithelial compartments (bulge, secondary hair germ) and co-express selected stem cell markers (Sox9, Tcf4 and Lgr5). Remarkably, Lhx2(+) cells represent the vast majority of cells in the bulge and secondary hair germ that proliferate in response to skin injury. This is functionally important, as wound re-epithelization is significantly retarded in heterozygous Lhx2 knockout (+/-) mice, whereas anagen onset in the HFs located closely to the wound is accelerated compared with wild-type mice. Cell proliferation in the bulge and the number of Sox9(+) and Tcf4(+) cells in the HFs closely adjacent to the wound in Lhx2(+/-) mice are decreased in comparison with wild-type controls, whereas expression of Lgr5 and cell proliferation in the secondary hair germ are increased. Furthermore, acceleration of wound-induced anagen development in Lhx2(+/-) mice is inhibited by administration of Lgr5 siRNA. Finally, Chip-on-chip/ChIP-qPCR and reporter assay analyses identified Sox9, Tcf4 and Lgr5 as direct Lhx2 targets in keratinocytes. These data strongly suggest that Lhx2 positively regulates Sox9 and Tcf4 in the bulge cells, and promotes wound re-epithelization, whereas it simultaneously negatively regulates Lgr5 in the secondary hair germ and inhibits HF cycling. Thus, Lhx2 operates as an important regulator of epithelial stem cell activity in the skin response to injury.