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1
Chen, Hairong [Verfasser]. "Functional analysis of candidate regulatory genes in regulatory T cells / Hairong Chen". Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1032432594/34.
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Hodgkinson, Lisa Marie. "Matrix regulatory genes in the human lens". Thesis, University of East Anglia, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490590.
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Purpose: The proteinases that cells employ to regulate the matrix include members of the zinc metalloproteinases; expression is likely to influence both the normal and injured human lens, which in tum can affect a number of biological functions e.g. migration. The current study therefore aimed to determine expression profiles in distinct regions ofthe human lens and following mechanical injury. Methods: For specific gene expression analyses the native human lens was dissected into three regions, using sham cataract surgical methods. Primary lens epithelial cell culture provided cells for analysis as a wounded lens system. Native lens capsular bags (CB) were cultured to assess short term wounding responses and ex vivo CBs (obtained with implanted intraocular lenses from cataract surgery sometime prior to death), were analysed to study the long term wounding responses. Total RNA extraction and reverse transcription technologies were developed for real time polymerase chain reaction amplification gene expression analysis. Protein expression was investigated using Western blotting techniques. Results: In the native lens, the overall MMP gene expression was low, while TIMP expression was high. Of the MMP family members, MTI-MMP was the most highly expressed in the epithelium, while MT2-MMP was the most abundant gene in the fibre cells. Moreover, the presence of unprocessed and activated MTI and MT2-MMP were confirmed by Western blotting. Selected adamalysin genes (ADAM-9, -10, -15 and -17) were highly expressed by all native lens regions. In the wounded lens and ex vivo samples transdifferentiation marker expression; alpha smooth muscle actin and fibronectin, was consistent with the different stages following cataract surgery. Significant elevation of specific gene expression was observed follo~ving injury, such as MMP-2, MMP-9, ADAM-9, ADAM-IS and ADAMTS-3. Conclusions: The present study demonstrates that regional distribution of MMPs, TIMPs, ADAMs and ADAMTSs occurs within the human lens. In the native lens expression of matrix degrading proteinases is generally low, while inhibitor expression is high. Following surgical injury, a significant increase in levels of specific genes, such as MMP-2 is observed; these particular genes are therefore likely to play key roles in the wound healing process after cataract surgery and are thus logical subjects for further investigation.
3
Coll-Lladó, Clara. "Evolution of muscle regulatory genes in chordates". Thesis, University of St Andrews, 2016. http://hdl.handle.net/10023/16136.
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Uprety, Bhawana. "Transcriptional Regulatory Mechanisms of Ribosomal Protein Genes". OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1080.
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Ribosomal protein genes are crucial for ribosome biogenesis. The ribosome itself is responsible for protein synthesis and hence cellular growth and development. Intertwining network of proteins in conjugation with cellular environment such as nutrition and growth factors collectively regulate expression of the ribosomal protein genes. DNA microarray analysis has implicated the role of 26S proteasome in transcriptional regulation of the ribosomal protein genes tying protein degradation to protein synthesis pathway. To determine the mechanism as to how the 26S proteasome promotes transcription of the ribosomal protein genes a series of experiments were performed. The results reveal that the 19S subcomplex of the 26S proteasome is recruited to the promoters of the ribosomal protein genes in a TOR (Target of Rapamycin)-dependent manner. TOR signals environmental cues and controls the expression of the ribosomal protein genes. Thus recruited 19S proteasome subcomplex promotes transcriptional initiation via facilitation of the recruitment of co-activator NuA4 (Nucleasome acetyltransferase of histone H4) complex to activator Rap1. NuA4 enhances PIC (Pre-initiation complex) formation at the core promoter, but it is not clearly understood how does it do so. Researches have identified two different forms of TBP: TAF (TBP associated factor)-dependent form of TBP and TAF-independent form of TBP. This work shows that impaired association of NuA4 interferes with TFIID recruitment, but recruits TAF-independent form of TBP to the core promoter. This recruitment of TBP is dependent on SAGA (Spt-Ada-Gcn5-acetyltransferase). Like ribosomal protein genes, antisense transcription is also enhanced by TAFs. However, it remains unknown whether NuA4 also promotes TAF-regulated antisense transcription. The results illustrate that like ribosomal protein genes, transcription of GAL10 antisense is also promoted by NuA4 HAT (histone acetyl transferase). NuA4 HAT is recruited to the 3’-end of the GAL10 coding sequence, acetylates histone H4 and promotes GAL10 antisense transcription. This work also reveals the roles of other chromatin regulatory factors in controlling antisense transcription. Collectively, these results significantly advance our current understanding of the regulatory mechanisms of ribosomal protein genes’ expression and antisense transcription. The ribosome and antisense are involved in virtually all the biological processes. Aberrant expression of the ribosomal protein genes and antisense transcripts are associated with numerous human disorders including cancers and cardiovascular diseases. Therefore, analyses of their regulatory processes provide valuable information toward understanding the etiology of numerous human diseases with potential therapeutic interventions.
5
Chan, Ping-kei. "The study of the regulatory elements of the human [beta]-globin gene". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31999062.
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Chan, Ping-kei, i 陳炳基. "The study of the regulatory elements of the human {221}-globin gene". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31999062.
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Nora, Fabiana Roos. "Interactions between regulatory genes required for meristem development". Thesis, University of East Anglia, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432435.
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Zhang, Yongquan. "Regulatory elements controlling the expression of OR37 genes". [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:100-opus-2272.
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Aagaard, Jan Erik. "Evolution of floral regulatory genes in the Lamiales /". view abstract or download file of text, 2004. http://wwwlib.umi.com/cr/uoregon/fullcit?p3136400.
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Thesis (Ph. D.)--University of Oregon, 2004.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-104). Also available for download via the World Wide Web; free to University of Oregon users.
10
Guo, Xiumei. "Regulatory and functional study of human cytoglobin". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3860145X.
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Chen, Di. "Regulatory pathways controlling larval development in caenorhabditis elegans". Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3144405.
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Tay, Yii Van. "Fates of genes after duplication : sublocalization and regulatory neofunctionalization". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44264.
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Kenyon, Julie R. "An analysis of upstream regulatory regions of retinal genes". Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268141.
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Carter, D. P. F. "Long-range functional interactions between genes and regulatory elements". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597329.
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The mouse b-globin locus contains four genes that are expressed throughout development in the same order they are arranged along chromosome 7. Upstream of the genes is a powerful regulatory element called the locus control region (LCR). The LCR is absolutely required for high-level expression of the b-globin genes. The models to explain how LCRs (and enhancers in general) are able to activate expression of the genes fall into two categories: contact and non-contact. The contact models propose that the LCR and the gene form a physical interaction that leads to active transcription. The non-contact models propose that the LCR alters the chromatin topology or nuclear organisation of the locus, or acts as a nucleation point for factors that polymerise along the chromatin fibre to activate the gene. A contact model has been inferred from indirect observations, in vitro experiments, and oversimplified assumptions. In the absence of a physical assay that is able to determine the three-dimensional arrangements of the b-globin locus the mechanisms of LCR activation remains open to speculation. In this thesis I describe the development of a novel technique called RNA tagging and recovery of associated proteins (RNA TRAP). RNA TRAP uses the power of RNA FISH to target an enzyme to the site of a specific actively transcribing gene. The enzyme catalayses the deposition of a biotin tag onto the chromatin in the vicinity of transcription, which acts as a handle to isolate and identify chromatin elements in proximity to the actively transcribed gene. Using RNA TRAP I have shown that elements of the LCR are in significantly physical proximity to the genes they activate in vivo. This is the first physical demonstration of the interaction of the LCR with a gene, and gives insight into the regulation of genes by enhancers.
15
Oudelaar, A. Marieke. "The three-dimensional regulatory landscapes of the globin genes". Thesis, University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:6cd793fe-b28a-4d98-a588-b6eec5dfa416.
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One of the most important outstanding questions in biology involves the precise spatial and temporal regulation of gene activity, which enables different cell types to express the specific set of genes required for their function and is therefore a cornerstone for complex biological life. Cis-regulatory elements, such as gene promoters and enhancers, play a key role in controlling gene activity. These elements physically interact with the genes they regulate within structural chromatin domains. The organisation of chromosomes into these domains is critical for specific regulation of gene expression and disruption of these structures underlies common human disease. However, it is not understood how chromatin domains form, how interactions between the cis-regulatory elements contained within them are established, or how such interactions influence gene expression. The major hurdles in addressing these questions are to determine chromatin structures with high resolution and sensitivity and to examine their dynamic nature within single cells. To overcome these, I have developed Tri-C, a new chromosome conformation capture assay that can analyse concurrent chromatin interactions at single alleles at high resolution. By combining Tri-C with conventional chromosome conformation capture techniques, I have analysed the three-dimensional regulatory landscapes of the well-characterised murine globin loci at unprecedented depth. Additionally, to examine the roles of cis-regulatory elements in establishing chromatin architecture, I have analysed how engineered deletions in enhancers and CTCF-binding elements in the murine alpha-globin locus disrupt its chromatin landscape. These analyses reveal that the chromatin domains containing the globin genes represent compartmentalised structures, which are delimited by CTCF boundaries. The heterogeneity of interactions in these domains between individual cells is indicative for a dynamic process of loop extrusion underlying their formation. Within chromatin domains, preferential structures are formed in which multiple enhancers and promoters interact simultaneously. These complexes provide a structural basis for understanding how multiple cis-regulatory elements cooperate to establish robust regulation of gene expression. Importantly, these complex, tissue-specific structures, cannot be explained by loop extrusion alone and indicate other, independent mechanisms contributing to chromosome architecture, likely involving interactions mediated by multi-protein complexes. Together, these analyses show that the current view of genome organisation, in which chromosomes are organised by stable loops and domains that self-assemble into hierarchical structures, is not correct. Rather, chromatin architecture reflects a complex interplay between distinct molecular mechanisms contributing to the formation of regulatory landscapes that facilitate precise, robust control of gene expression.
16
Furchtgott, Leon A. "Simultaneous Inference of Cell Types, Lineage Trees, and Regulatory Genes From Gene Expression Data". Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493563.
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Important goals of developmental biology include identifying cell types, understanding the sequence of lineage choices made by multipotent cells and unconvering the molecular networks controlling these decisions. Achieving these goals through computational analysis of gene expression data has been difficult. In this dissertation supervised by Sharad Ramanathan, I develop a probabilistic framework to identify cell types, infer lineage relationships and discover core gene networks controlling lineage decisions. Working with Sandeep Choubey and Sumin Jang, we infer the gene expression dynamics of early differentiation of mouse embryonic stem cells, revealing discrete state transitions across nine cell states. Using a probabilistic model of the gene regulatory networks, we predict that these states are further defined by distinct responses to perturbations and experimentally verify three such examples of state-dependent behavior. Working with Vilas Menon and Sam Melton, we infer a lineage tree for early neural development and putative regulatory transcription factors from single-cell transcriptomic profiles. The lineage tree shows a prominent bifurcation between cortical and mid/hindbrain cell types, and the inferred lineage relationships were confirmed by clonal analysis experiments. In summary, this study provides a framework to infer predictive models of the gene regulatory networks that drive cell fate decisions.Biophysics
17
Dash, Bhagirathi. "Molecular cloning and characterization of important stress and redox regulatory genes from Hydra vulgaris". Texas A&M University, 2005. http://hdl.handle.net/1969.1/4994.
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In this research, important stress and redox regulatory genes present in
Hydra vulgaris were isolated and characterized to facilitate our understanding of
the evolution and mechanisms of stress response. H. vulgaris heat shock protein
70 (HvHSP70), extracellular copper zinc superoxide dismutase (HvECCuZnSOD),
manganese superoxide dismutase (HvMnSOD), phospholipid
peroxidase glutathione peroxidase (HvPHGPx) and monofunctional catalase
(HvCatalase) were cloned and characterized with regard to stress response,
phylogeny and molecular structure.
The HSP70 gene isolated from H. vulgaris encodes a polypeptide of 650
amino acids (Mw=710,037) and is interrupted by three intron sequences. The 5'
non-coding region of the HvHSP70 possessed the canonical heat shock
elements. Phylogenetically HvHSP70 formed a distinct lineage. A molecular
model generated for the N-terminal fragment of the HvHSP70 displayed the heat
shock protein fold and domains of phosphotransferases. The EC-CuZnSOD cDNA isolated from H. vulgaris encodes a protein of
189 amino acids (Mw=20959.73); the first 19 amino acids constitute the
presumed signal peptide. Phylogenetically HvEC-CuZnSOD is grouped with ECCuZnSODs
from several organisms. A molecular model generated for the
HvEC-CuZnSOD displayed the CuZnSOD (beta)-barrel fold.
The MnSOD cDNA isolated from H. vulgaris encodes a protein of 219
amino acids (Mw=24348.75); the first 21 amino acids constitute the presumed
mitochondria-targeting signal peptide. Phylogenetically HvMnSOD is clustered
with mollusk and crustacean MnSODs. A molecular model generated for the
HvMnSOD displayed the N-terminal long alpha antiparallel hairpin and the Cterminal
mixed alpha/beta fold characteristic of MnSODs.
The PHGPx gene isolated from H. vulgaris encodes a polypeptide of 168
amino acids (Mw=18746.51) including a TGA-encoded selenocysteine at residue
44 and lacks any intron. Phylogenetically HvPHGPx is grouped with PHGPxs
from several organisms. A molecular model generated for the HvPHGPx
displayed the thioredoxin fold.
The 3'-end of a cDNA sequence encoding for 168 amino acids of the Cterminal
end of a catalase was isolated from H. vulgaris. Phylogenetically
HvCatalase is grouped with heme-containing monofunctional catalases.
Hydrae exposed to thermal, starvation, oxidative and metal stress
responded by regulating respective mRNA transcriptions suggesting that these genes are involved in stress and (anti)oxidative processes and may have
potential as molecular biomarkers for assessing aquatic environment quality.
18
Borba, Ana Rita Andrade. "Transcriptional regulatory mechanisms controlling key genes involved in C4 photosynthesis in maize". Doctoral thesis, Universidade Nova de Lisboa, Instituto de Tecnologia Química e Biológica António Xavier, 2019. http://hdl.handle.net/10362/94108.
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"Global food security is under threat due to global warming and population
growth. This alarming scenario could however be mitigated by increasing crop
yield potential through photosynthesis improvement. Although plants performing
the C3-type of photosynthesis (e.g. rice and wheat) are the most abundant
and well-characterised in terms of their biology, biochemistry, and physiology,
C4 plants (e.g. maize and sugarcane) are generally more efficient than C3 in
capturing carbon dioxide (CO2) and producing biomass in high-temperature
and drought conditions.(...)"N/A
19
Moses, Daniel. "Regulatory Elements, Protein Function and Evolution of the Actinodin Genes". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26216.
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Small fibrils termed actinotrichia are involved with the growth and structure of the fin fold during fin development in fish. The actinodin (and) genes are required for actinotrichia formation, and the loss of these genes from the genomes of tetrapods has been implicated in the tetrapod-specific loss of actinotrichia, loss of a fin fold and the concurrent evolution of paired fins into limbs. This study focuses on the function of the and genes and their role in actinotrichia formation. The results reveal cis-acting regulatory elements required for and1 expression in the fin epithelium. Furthermore, it is shown that the And proteins display similarities to the secreted signaling molecule, Ecrg4, implying a possible role in cell differentiation during fin fold development. In the final section of this report, I use a genomic analysis to show that the and genes were lost from otherwise well-conserved syntenic loci in fish and tetrapod genomes. These results suggest possible causes for the evolutionary loss of and genes and the associated developmental changes that may have permitted fin to limb evolution.
20
Ketterling, Matthew Gene. "Quantitative analysis of CIS-regulatory sequences in genes of arabidopsis". [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0001266.
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Guo, Xiumei, i 郭秀梅. "Regulatory and functional study of human cytoglobin". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B3860145X.
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Zhang, Wei, i 张伟. "Characterization of distal and proximal regulatory elements of the human neuroglobin gene". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47147568.
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Garrett, Christine. "Functional mapping of pea legumin upstream regulatory elements using TI plasmid vectors". Thesis, Durham University, 1991. http://etheses.dur.ac.uk/6041/.
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The leg A gene from Pisum sativum L. has been extensively characterised and a distinct pattern of developmental and organ-specific gene expression demonstrated. Homology between legumin genes from other species has given some indication of those sequences which may be responsible for the regulation at the level of transcription. This study was designed to provide a functional analysis of the upstream sequences. A number of plasmid vectors containing a maximum of 1.2 kb of upstream sequence from the leg A gene of Pisum sativum I., ligated to the coding region of the nopaline synthase (nos) gene, were constructed. The use of smaller promoter fragments and the insertion of spacer DNA within the promoter region was employed in an effort to localise the regions of 5' flanking sequence which may play a role in tissue specific expression. In a minority of tumours derived from tissue transformed with the vector containing the ' full-length ' leg A promoter, low levels of nopaline were detected, but not with those containing a shorter promoter fragment. Results from the analysis of Seed tissue indicates that 800 bp of the leg A promoter was insufficient to direct tissue-specific expression of the fused nopaline synthase gene in transgenic Nicotiana tabacum, although one individual plant showed a constitutive pattern of nopaline synthesis. However, published results obtained with legumin and other storage protein gene promoters would suggest that this promoter fragment should have been sufficient to confer seed-specific expression. This suggests that there may have been undesirable secondary structures, or small undetected rearrangements, introduced during the construction of the transcriptional fusions between leg A and nos. Alternatively the marker gene may be inadequately sensitive to permit detection of low levels of expression.
24
Pati, Amrita. "Modeling and Analysis of Regulatory Elements in Arabidopsis thaliana from Annotated Genomes and Gene Expression Data". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/44132.
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Modeling of cis-elements in the upstream regions of genes is a challenging computational problem. A set of regulatory motifs present in the promoters of a set of genes can be modeled by a biclique. Combinations of cis-elements play a vital role in ascertaining that the correct co-action of transcription factors binding to the gene promoter, results in appropriate gene expression in response to various stimuli. Geometrical and spatial constraints in transcription factor binding also impose restrictions on order and separation of cis-elements. Not all regulatory elements that coexist are biologically significant. If the set of genes in which a set of regulatory elements co-occur, are tightly correlated with respect to gene expression data over a set of treatments, the regulatory element combination can be biologically directed.
The system developed in this work, XcisClique, consists of a comprehensive infrastructure for annotated genome and gene expression data for Arabidopsis thaliana. XcisClique models cis-regulatory elements as regular expressions and detects maximal bicliques of genes and motifs, called itemsets. An itemset consists of a set of genes (called a geneset) and a set of motifs (called a motifset) such that every motif in the motifset occurs in the promoter of every gene in the geneset. XcisClique differs from existing tools of the same kind in that, it offers a common platform for the integration of sequence and gene expression data. Itemsets identified by XcisClique are not only evaluated for statistical over-representation in sequence data, but are also examined with respect to the expression patterns of the corresponding geneset. Thus, the results produced are biologically directed. XcisClique is also the only tool of its kind for Arabidopsis thaliana, and can also be used for other organisms in the presence of appropriate sequence, expression, and regulatory element data. The web-interface to a subset of functionalities, source code and supplemental material are available online at http://bioinformatics.cs.vt.edu/xcisclique.Master of Science
25
Webber, Aaron. "Transcriptional co-regulation of microRNAs and protein-coding genes". Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/transcriptional-coregulation-of-micrornas-and-proteincoding-genes(f5b601b2-33f3-4608-9ae8-b7d5a0c6beaf).html.
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This thesis was presented by Aaron Webber on the 4th December 2013 for the degree of Doctor of Philosophy from the University of Manchester. The title of this thesis is ‘Transcriptional co-regulation of microRNAs and protein-coding genes’. The thesis relates to gene expression regulation within humans and closely related primate species. We have investigated the binding site distributions from publically available ChIP-seq data of 117 transcription regulatory factors (TRFs) within the human genome. These were mapped to cis-regulatory regions of two major classes of genes, 20,000 genes encoding proteins and 1500 genes encoding microRNAs. MicroRNAs are short 20 - 24 nt noncoding RNAs which bind complementary regions within target mRNAs to repress translation. The complete collection of ChIP-seq binding site data is related to genomic associations between protein-coding and microRNA genes, and to the expression patterns and functions of both gene types across human tissues. We show that microRNA genes are associated with highly regulated protein-coding gene regions, and show rigorously that transcriptional regulation is greater than expected, given properties of these protein-coding genes. We find enrichment in developmental proteins among protein-coding genes hosting microRNA sequences. Novel subclasses of microRNAs are identified that lie outside of protein-coding genes yet may still be expressed from a shared promoter region with their protein-coding neighbours. We show that such microRNAs are more likely to form regulatory feedback loops with the transcriptional regulators lying in the upstream protein-coding promoter region. We show that when a microRNA and a TRF regulate one another, the TRF is more likely to sometimes function as a repressor. As in many studies, the data show that microRNAs lying downstream of particular TRFs target significantly many genes in common with these TRFs. We then demonstrate that the prevalence of such TRF/microRNA regulatory partnerships relates directly to the variation in mRNA expression across human tissues, with the least variable mRNAs having the most significant enrichment in such partnerships. This result is connected to theory describing the buffering of gene expression variation by microRNAs. Taken together, our study has demonstrated significant novel linkages between the transcriptional TRF and post-transcriptional microRNA-mediated regulatory layers. We finally consider transcriptional regulators alone, by mapping these to genes clustered on the basis of their expression patterns through time, within the context of CD4+ T cells from African green monkeys and Rhesus macaques infected with Simian immunodeficiency virus (SIV). African green monkeys maintain a functioning immune system despite never clearing the virus, while in rhesus macaques, the immune system becomes chronically stimulated leading to pathogenesis. Gene expression clusters were identified characterizing the natural and pathogenic host systems. We map transcriptional regulators to these expression clusters and demonstrate significant yet unexpected co-binding by two heterodimers (STAT1:STAT2 and BATF:IRF4) over key viral response genes. From 34 structural families of TRFs, we demonstrate that bZIPs, STATs and IRFs are the most frequently perturbed upon SIV infection. Our work therefore contributes to the characterization of both natural and pathogenic SIV infections, with longer term implications for HIV therapeutics.
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Smeds, Johanna. "Role of the CDKN2A and related cell cycle regulatory genes in melanoma and other human cancers /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-105-5/.
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Svingen, Terje, i n/a. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity". Griffith University. School of Biomolecular and Biomedical Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20050830.135356.
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Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.
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Svingen, Terje. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity". Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365774.
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Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
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Smart, James. "A partial characterization of three photosynthetic regulatory genes in Rhodobacter capsulatus". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61681.pdf.
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Lim, Jeong-Eun. "Regulatory genetic variants in mental illness focus on serotonin-related genes /". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1196198735.
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Griffiths, Marcus. "Identifying wheat root traits and regulatory genes for nitrogen uptake efficiency". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/48611/.
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Wheat (Triticum spp.) is a particularly important crop for food security, providing 20% of worldwide calorie intake. Food production is not meeting the projected global demand of an increase of 2.4% p.a. Improvement of resource capture in wheat could help meet this demand. Nitrogen (N) is an essential macronutrient for plant growth and development; however, nitrogen use efficiency (NUE) for cereal production is only 33%. Domestication of modern varieties of wheat may have lost potentially beneficial agronomic traits, particularly in the root system. Optimisation of root system architecture could profoundly improve nitrogen uptake efficiency (NUpE) and in turn increase the yield potential of the crop. Using ancestral wheat germplasm and mapping populations, desirable traits may be identified and bred back into commercial wheat varieties to increase yield potential. Using a high-throughput hydroponic root phenotyping system, N-dependent root traits have been identified in wheat mapping populations. Using transcriptomic analyses, the gene expression profile of a candidate N-dependent root QTL has been identified. Using a new root phenotyping system, X-ray micro-computed tomography (μCT), a three-dimensional representation of wheat roots can now be imaged in soil. A selection of the same mapping lines have been used for 3D μCT analysis based on field NUpE parameters to identify promising root traits in both seedlings and mature plants.
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Bahirwani, Vishal. "Exploring transcription patterns and regulatory motifs in Arabidopsis thaliana". Thesis, Manhattan, Kan. : Kansas State University, 2010. http://hdl.handle.net/2097/4194.
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Basford, Joshua E. "Colinear Expression of the Mouse HoxB Cluster: Potential Regulatory Role of Histone H4 Acetylation". University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin997988435.
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Mejías, Luque Raquel. "Regulatory effects of pro-inflammatory cytokines on genes associated with gastric carcinogenesis". Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7156.
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El patró específic d'expressió de glicosiltransferases i antígens Lewis observat a la mucosa gàstrica normal es perd durant el procés de la carcinogènesi gàstrica. Aquí descrivim que canvis en l'expressió dels antígens Lewis en cèl·lules HT-29/M3 de càncer de còlon induïts per la transfecció del cDNA de FUT1 resulten en un fenotip menys invasiu i menys metastàtic.La gastritis crònica produïda per la infecció per Helicobacter pylori és un dels principals determinants en la patogènesi del càncer gàstric, i comporta nivells elevats de citoquines proinflamatòries com TNF-α, IL-1β o IL-6, que poden regular l'expressió de gens implicats en la transformació neoplàsica gàstrica. Vam analitzar l'efecte de citoquines proinflamatòries en l'expressió de glicosiltransferases i antígens Lewis en cèl·lules de càncer gàstric va ser analitzat i vam observar que el tractament d'aquestes cèl·lules amb IL-1β augmentava l'expressió d'antígens Lewis de tipus 2. A més, vam observar que tumors gàstrics amb inflamació crònica presentaven nivells més elevats d'estructures glicosídiques de tipus 2, suggerint que determinades glicosiltransferases podrien estar regulades per la inflamació.
Els adenocarcinomes gàstrics de tipus intestinal s'originen a partir d'una sèrie successiva de lesions precanceroses que porten a una transdiferenciació intestinal de la mucosa gàstrica. En aquest procés s'activa l'expressió de diferents gens intestinals a les cèl·lules gàstriques, com és el cas dels gens de les mucines intestinals MUC2 i MUC4 i del factor de transcripció intestinal CDX2. Nosaltres vam estudiar l'efecte de citoquines inflamatòries i de les seves vies de senyalització associades en l'expressió d'aquests gens va ser estudiat. El primer que vam constatar va ser que IL-6 regulava l'expressió de MUC4 a través de la via de gp130/STAT3 a línies cel·lulars de càncer gàstric, mentre que l'expressió de MUC2 era induïda per TNF-α a través de la via de senyalització de NF-κB. A més, vam observar que l'expressió de CDX2 no era regulada per citoquines inflamatòries. Finalment, vam trobar que les diferències en l'expressió de les mucines intestinals MUC2 i MUC4 a tumors gàstrics podien ser explicades per diferències en el tipus d'inflamació predominant.
De tots aquests resultats podem concloure que la inflamació i les vies de senyalització associades modulen l'expressió de gens associats a la carcinogènesi gàstrica.
In the gastric carcinogenetic process the specific expression pattern of glycosyltransferases and Lewis antigens displayed by the normal gastric mucosa is lost. We detected that changes in the expression of Lewis antigens induced by the transfection of FUT1 cDNA in HT-29/M3 cells determined a less invasive and metastatic phenotype.
Chronic gastritis caused by H. pylori infection is a major determinant in the pathogenesis of gastric cancer, and present increased levels of the pro-inflammatory cytokines TNF-α, IL-1β and IL-6, which can regulate the expression of genes involved in the gastric neoplastic transformation. We analysed the effect of pro-inflammatory cytokines on the expression of glycosyltransferases and Lewis antigens in gastric cancer cells. IL-1β treatment increased the expression of type 2 Lewis antigens, and, in addition, we observed that gastric tumours with chronic inflammation displayed increased levels of type 2 glycan structures, suggesting that specific glycosyltransferases may be regulated by inflammation.
Intestinal-type gastric adenocarcinomas develop from successive pre-cancerous lesions that lead to an intestinal transdifferentiation of the gastric mucosa. In this process many intestinal genes are activated in gastric cells, such as the intestinal mucin MUC2 and MUC4 genes and the transcription factor CDX2. We studied the effect of pro-inflammatory cytokines and their associated signalling pathways on the expression of these genes. IL-6 regulated the expression of MUC4 through the gp130/STAT3 signalling pathway in gastric cancer cell lines, while MUC2 expression was induced by TNF-α through the NF-κB signalling pathway. No effects on CDX2 expression were observed after cytokine treatment in gastric tumour cells. Finally, we found that the differences observed in the expression of the intestinal mucins MUC2 and MUC4 in gastric tumours could be explained by differences in the predominant type of inflammation present in gastric adenocarcinomas.
In conclusion, our results suggest that inflammation and its associated signalling pathways modulate the expression of genes associated with gastric carcinogenesis.
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Lundmark, Frida. "Genetic analysis of IL7R and other immune-regulatory genes in multiple sclerosis /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-278-1/.
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Sun, Lei. "Biodiversity of transporter and regulatory genes involved in dimethylsulphoniopropionate catabolism in bacteria". Thesis, University of East Anglia, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.514337.
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Bitton, Danny Asher. "Discovery of Novel Protein Coding Genes and Antisense Regulatory Transcripts in Eukaryotes". Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.532201.
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Alcock, Rachael A. "Role of cell death regulatory genes and radiation response in pancreatic adenocarcinomas". Thesis, University of Central Lancashire, 2002. http://clok.uclan.ac.uk/1745/.
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Gene expression studies have revealed that there is more than one cellular pathway governing growth inhibition and apoptosis. Mutations in the ras oncogene that(activate ras) are known to lead to the inactivation of genes that are directly involved in these pathways of growth inhibition and apoptosis. Oncogenic activated ras inhibits TGF-P signalling through the down-regulation of RII expression and abrogates apoptotic pathways through down-modulation of PAR-4 gene expression. A majority of pancreatic turnours harbour K-ras point mutations and these mutations dysregulate, the growth inhibition and apoptosis processes. This leads us to hypothesize that K-ras mutant phenotype status in pancreatic turnours will alter the expression of the RII and PAR-4 genes, and would further dysregulate growth inhibitory and apoptotic processes. In this study, the majority of pancreatic turnours showed down-regulation of RII and PAR-4 gene expression. A strong correlation of down-regulation of RII and PAR-4 with K-ras mutational status was observed. In particular, down regulation of PAR-4 correlated with poor survival in patients with pancreatic adenocarcinomas. Blocking the function of oncogenic ras by using a famesyltransferase inhibitor (Frl) restored RII expression and TGF-P signalling, and this caused enhanced sensitivity of cell lines to radiation. The restoration of RH function by FrI was linked to down-modulation of DNA methyltransferase enzyme that is often implicated in hypermethylation of promoters. Over-expression of RII in pancreatic tumour cells led to the restoration of TGF-P signalling and enhancement of radiation sensitivity. Induction of the pro-apoptotic effector gene, bav (bcI-2 family member) by radiation in RII over-expressed pancreatic cancer cells, was found to be a key mechanism involved in radiation sensitivity. Overexpression of PAR-4 sensitized the cells to radiation and this sensitization was linked to down-modulation of radiation induced Bcl-2 protein. Together, these findings strongly suggest that the restoration of function of the key growth inhibitory and cell death genes RII and PAR-4, which are affected by oncogenic ras mutations in pancreatic turnours will restore and enhance cellular responses to radiation induced clonogenic inhibition and apoptosis.
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Mootien, Saraspadee. "New pleiotropic regulatory genes for antibiotic production in Streptomyces coelicolor A3(2)". Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327543.
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Blacha, Anna Maria. "Investigating the role of regulatory genes in heterosis for superior growth and biomass production in Arabidopsis thaliana". Phd thesis, Universität Potsdam, 2009. http://opus.kobv.de/ubp/volltexte/2010/4614/.
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‘Heterosis’ is a term used in genetics and breeding referring to hybrid vigour or the superiority of hybrids over their parents in terms of traits such as size, growth rate, biomass, fertility, yield, nutrient content, disease resistance or tolerance to abiotic and abiotic stress.
Parental plants which are two different inbred (pure) lines that have desired traits are crossed to obtain hybrids. Maximum heterosis is observed in the first generation (F1) of crosses. Heterosis has been utilised in plant and animal breeding programs for at least 90 years: by the end of the 21st century, 65% of worldwide maize production was hybrid-based. Generally, it is believed that an understanding of the molecular basis of heterosis will allow the creation of new superior genotypes which could either be used directly as F1 hybrids or form the basis for the future breeding selection programmes.
Two selected accessions of a research model plant Arabidopsis thaliana (thale cress) were crossed to obtain hybrids. These typically exhibited a 60-80% increase of biomass when compared to the average weight of both parents. This PhD project focused on investigating the role of selected regulatory genes given their potentially key involvement in heterosis.
In the first part of the project, the most appropriate developmental stage for this heterosis study was determined by metabolite level measurements and growth observations in parents and hybrids. At the selected stage, around 60 candidate regulatory genes (i.e. differentially expressed in hybrids when compared to parents) were identified. Of these, the majority were transcription factors, genes that coordinate the expression of other genes. Subsequent expression analyses of the candidate genes in biomass-heterotic hybrids of other Arabidopsis accessions revealed a differential expression in a gene subset, highlighting their relevance for heterosis. Moreover, a fraction of the candidate regulatory genes were found within DNA regions closely linked to the genes that underlie the biomass or growth heterosis. Additional analyses to validate the role of selected candidate regulatory genes in heterosis appeared insufficient to establish their role in heterosis. This uncovered a need for using novel approaches as discussed in the thesis.
Taken together, the work provided an insight into studies on the molecular mechanisms underlying heterosis. Although studies on heterosis date back to more than one hundred years, this project as many others revealed that more investigations will be needed to uncover this phenomenon.„Heterosis“ ist ein in der Genetik und der Züchtung verwendeter Begriff, der die Hybridwüchsigkeit oder die Überlegenheit der Hybriden über ihre Eltern in Bezug auf Eigenschaften wie Größe, Wachstumsrate, Biomasse, Fruchtbarkeit, Ertrag, Nährstoffgehalt, Widerstand gegen Krankheiten oder Toleranz in Bezug auf biotischen oder abiotischen Stress bezeichnet. Um Hybriden zu erzeugen, werden aus zwei verschiedenen Inzuchtlinien (reine Linien) bestehende Elternpflanzen, welche die gewünschten Eigenschaften besitzen, miteinander gekreuzt. Der stärkste Heterosiseffekt wird in der ersten Kreuzungsgeneration (F1) beobachtet. Heterosis wird in Pflanzen- und Tierzuchtprogrammen schon seit mindestens 90 Jahren genutzt. So beruhte zum Ende des 20. Jahrhunderts 65% der weltweiten Maisproduktion auf Hybridzüchtung. Es wird angenommen, dass ein Verständnis der molekularen Grundlagen der Heterosis die Schaffung neuer, überlegener Genotypen erlaubt, die dann direkt als F1-Hybriden verwendet, oder als Grundlage für zukünftige Zucht- und Selektionsprogramme dienen können. Zwei ausgewählte Akzessionen der Modellpflanze Arabidopsis thaliana (Ackerschmalwand) wurden miteinander gekreuzt, um Hybriden zu erzeugen. Verglichen mit dem durchschnittlichen Gewicht ihren beiden Elternlinien zeigten diese eine 60-80%ige Zunahme an Biomasse. Diese Doktorarbeit befasst sich damit, die Rolle ausgewählter, regulatorischer Gene und ihre mögliche Schlüsselrolle bei der Heterosis zu untersuchen. Im ersten Teil der Arbeit wurde anhand der Gehaltsbestimmung ausgewählter Stoffwechselprodukte und Wachstumsbeobachtungen bei den Eltern und Hybriden das günstigste Entwicklungsstadium für diese Heterosisstudie bestimmt. In diesem Entwicklungsstadium wurden ungefähr 60 regulatorische Gene (d.h. Expressionsunterschiede zwischen Hybriden und Elternlinien) als Kandidaten identifiziert. Ein Großteil dieser Kandidaten waren Transkriptionsfaktoren, also Gene, die die Expression anderer Gene regulieren. Die nachfolgende Expressionsanalyse dieser Kandidatengene in Biomasse-Heterosis Hybriden anderer Arabidopsis Akzessionen zeigte bei einem Teil dieser Gene Expressionsunterschiede, die ihre Bedeutung bei der Heterosis betonen. Darüber hinaus wurde ein Teil dieser regulatorischen Kandidatengene innerhalb von DNS-Regionen gefunden, die eng mit Biomasse- oder Wachstumsheterosis in Verbindung stehen, und somit ihre Wichtigkeit in Bezug auf Heterosis unterstreichen. Weitergehende Analysen um die Rolle dieser ausgewählten regulatorischen Kandidatengene bei der Heterosis aufzuklären, waren nicht aussagekräftig genug, um ihre Rolle bei der Heterosis zu bestätigen. In der Doktorarbeit wird die Notwendigkeit neue Wege zur Aufklärung der Heterosis zu finden, diskutiert. Zusammenfassend gibt diese Doktorarbeit einen Einblick über Studien der molekularen Mechanismen, die der Heterosis zugrunde liegen. Diese Arbeit zeigt, dass obwohl Heterosis bereits seit mehr als hundert Jahren studiert wird, weitere Untersuchungen zur Aufklärung dieses Phänomens notwendig sind.
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Ghosh, Priyanjali. "Investigating the Gene Regulatory Network Underlying Caudal Hindbrain Specification in Embryonic Zebrafish". eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/979.
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To understand the gene regulatory network (GRN) governing caudal hindbrain formation in embryonic zebrafish, several early expressed factors have been manipulated, and multiple genetic mutants have been characterized. Such analyses have identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Considering that the caudal hindbrain is relatively complex – for instance, unique sets of neurons are formed in each rhombomere segment – it is likely that additional essential genes remain to be identified and integrated into the caudal hindbrain GRN.
Our results reveal that r4 gene expression is unaffected by the individual loss of hoxb1b, hoxb1a or RA, but is under the combinatorial regulation of RA together with hoxb1b. In contrast, r5/r6 gene expression is dependent on RA, FGF, hnf1ba and valentino – as individual loss of these factors abolishes r5/r6 gene expression. Analysis of six mutant lines (gas6, gbx1, sall4, eglf6, celf2, and greb1l) did not reveal rhombomere or neuronal defects, but transcriptome analysis of one line (gas6 mutant) identified expression changes for genes involved in several developmental processes – suggesting that these genes may have subtle roles in hindbrain development.
We conclude that r4-r6 formation is relatively robust, such that very few genes are absolutely required for this process. However, there are mechanistic differences in r4 versus r5/r6, such that no single factor is required for r4 development while several genes are individually required for r5/r6 formation.
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Rahrami, Ahmad Reza. "Characterisation and manipulation of a plant proteasome subunit gene". Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340216.
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Engström, Pär. "Gene complexes and regulatory domains in metazoan genomes /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-361-0/.
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Ramdayal, Kavisha. "Incidence and Regulatory Implications of Single Nucleotide Polymorphisms among Established Ovarian Cancer Genes". Thesis, Online access, 2009. http://etd.uwc.ac.za/usrfiles/modules/etd/docs/etd_gen8Srv25Nme4_5111_1277754725.pdf.
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Thuraisingam, Thusanth. "Macrophage regulatory genes Nramp1 and MK2 : implication in inflammation and cutaneous wound healing". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111902.
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Macrophages are active participants in many important biological processes, including antimicrobial activity, tumour surveillance, apoptotic cell clearance, homeostasis and wound healing. The activity of all cells is under the direct influence of their genetic makeup and macrophages are no exception. Natural resistance-associated macrophage protein 1 (Nramp1, also known as SLC11A1) is a macrophage-restricted gene that confers resistance to intracellular pathogens in mice. Mitogen activated protein kinase activated protein kinase 2 (MAPKAPK-2 or MK2), a substrate of p38 MAPK, is known to influence the activation of macrophages in response to stressors, including the Toll-like receptor (TLR)-4 ligand LPS. Like NRAMP1, MK2 has also been shown to influence the efficiency of the antibacterial response. The present study evaluates the role of NRAMP1 and MK2 in TLR-mediated cytokine induction and their role in cutaneous wound healing. Mice lacking NRAMP1 are severely impaired in their rate of cutaneous wound healing. Nramp1 gene ablation has been associated with lower levels of SLPI, a protein previously demonstrated to influence the rate of wound healing in a non-redundant fashion. Macrophages derived from Nramp1-null mice are less efficient in activating p38 MAPK signaling, which results in lower levels of MK2 phosphorylation. The reduced level of p38 MAPK and MK2 activation in Nramp1-null macrophages also correlates with decreased cytokine induction in response to TLR7 ligand stimulation of these cells. Using p38 MAPK inhibitor and MK2-deficient macrophages, we demonstrate that TLR7- and TLR9-mediated cytokine induction is directly under the control of this signaling pathway. Furthermore, cytokine induction is regulated by MK2 at the post-transcriptional level. Macrophage-induced cytokines play an important role in cutaneous wound healing. Since MK2-deficient macrophages are severely impaired in their ability to induce cytokines following activation, we next evaluated the role of MK2 in cutaneous wound healing. Our results demonstrate that the rate of wound healing is significantly delayed in the absence of MK2. The level of cytokine expression in the wounds is impaired and macrophages are major players in cutaneous wound healing. Our data also show that intradermal transfer of macrophages with intact MK2 significantly improved wound healing kinetics. Overall, the studies presented in this dissertation demonstrate the importance of NRAMP1 and MK2 in the modulation of macrophage gene expression, and their important role in the control of cutaneous wound healing.
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Hayesmoore, Jesse B. G. "Investigation of cis-regulatory variation in candidate genes for psychiatric and neurodegenerative disease". Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55874/.
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In recent years, molecular genetics research has identified a large number of putative susceptibility genes for a variety of complex psychiatric and neurodegenerative disorders. However, in most instances, the particular functional variants involved have not been identified, and it is typically unclear by what mechanism the pathogenic effect is mediated. Where a genetic association does not appear to be fully explicable by variants that alter the amino acid sequence of a protein, it is a reasonable hypothesis that the association might be mediated by cis-acting variants that alter gene expression. This hypothesis was tested in this thesis in relation to 10 putative susceptibility genes for psychiatric and neurodegenerative disorders. The genes were DISCI, RELN, GABRA4, GABRA5, GABRB1, GABRB2, GABRG2, GABRG3, NOS1AP and MAPT. Each one of these genes was investigated by assays of relative allelic expression applied to a large number of post mortem human brain samples. Samples were also genotyped for relevant variants that had previously shown association with disease in order to test those variants for a putative cis-regulatory effect. Cis-regulatory variation manifested as unequal expression of each parental gene copy at the mRNA level was detected in nearly all of the genes in at least one tissue sample. However, for only two genes (RELN and MAPT) was evidence obtained that specific variants implicated in disease influenced expression.
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Coleman, Heather. "Analyses of coding and regulatory sequences for delayed-early genes of herpesvirus saimiri". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303950.
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Delaney, S. J. "Cis-acting regulatory elements of the larval serum protein-1 genes of Drosopila". Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/38282.
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Perrine, Kimberly Gayle. "Genetic analysis of regulatory and structural genes of nitrogen metabolism in Neurospora crassa /". The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487262513407313.
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Bali, Anish. "Cell cycle regulatory genes as markers of outcome in serious epithelial ovarian cancer". Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23173.
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