subject:(Gene regulation)

University of Georgia

1. Craven, Sarah Hope. Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1.

Degree: PhD, Microbiology, 2009, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/craven_sarah_h_200908_phd

► Multiple mechanisms regulate aromatic compound degradation in the soil bacterium Acinetobacter baylyi ADP1. Herein, complementary mechanisms controlling the consumption of benzoate are explored: 1) transcriptional… (more)

▼ Multiple mechanisms regulate aromatic compound degradation in the soil bacterium Acinetobacter baylyi ADP1. Herein, complementary mechanisms controlling the consumption of benzoate are explored: 1) transcriptional regulation and 2) chromosomal amplification of catabolic genes. The former highlights BenM, a member of the LysR family of regulators controlling transcription of a complex regulon for benzoate degradation in ADP1. BenM activates gene expression in response to two effectors, benzoate and muconate. These effectors act synergistically to allow high-level gene expression, a feature not characterized in any other member of this broad family. Here, the unique effector profile of BenM is explored. Genetic studies, combined with structural work, elucidate the role of two distinct effector-binding sites in BenM. Targeted mutagenesis confirms the physiological relevance of a hydrophobic benzoate binding pocket and pinpoints critical residues, Arg160 and Tyr293, essential for benzoate-dependent gene expression and synergistic transcriptional activation. BenM variants that activate transcription in the absence of inducer are examined: BenM(R156H), BenM(R225H), and BenM(E226K). Structural studies of BenM variants reveal subtle conformational changes associated with transcriptional activation. The recent discovery of gene amplification in ADP1 highlights an alternate strategy of genetic regulation. In strains lacking wild-type regulation, chromosomal amplification of catabolic genes can compensate for low transcript levels. Here, a wide spectrum of amplification events were studied using multiple approaches uniquely available in the tractable ADP1 model system. Approximately 50 amplification mutants with enhanced benzoate catabolism were characterized. Each harbors multiple copies of a genomic region, ranging from 12 kbp to more than 300 kbp, encompassing the ben and cat functional genes. Analysis of the precise sequence at amplicon endpoints identifies the DNA sequence involved in formation of the original duplication. In all cases examined, these sequences indicate genetic duplication was initiated by a homology-independent illegitimate recombination mechanism. Recurrence of exact duplication junctions in multiple mutants reveals site preference in duplication formation, a mechanism we designate position-specific illegitimate recombination. The novel experimental tools developed here will facilitate a rapid and thorough examination of the full spectrum of gene amplification events contributing to ADP1 genome plasticity, as well as enable studies into the relevant recombination mechanisms. Advisors/Committee Members: Ellen L. Neidle.

Subjects/Keywords: Gene regulation

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APA (6^th Edition):

Craven, S. H. (2009). Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/craven_sarah_h_200908_phd

Chicago Manual of Style (16^th Edition):

Craven, Sarah Hope. “Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1.” 2009. Doctoral Dissertation, University of Georgia. Accessed July 16, 2019. http://purl.galileo.usg.edu/uga_etd/craven_sarah_h_200908_phd.

MLA Handbook (7^th Edition):

Craven, Sarah Hope. “Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1.” 2009. Web. 16 Jul 2019.

Vancouver:

Craven SH. Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1. [Internet] [Doctoral dissertation]. University of Georgia; 2009. [cited 2019 Jul 16]. Available from: http://purl.galileo.usg.edu/uga_etd/craven_sarah_h_200908_phd.

Council of Science Editors:

Craven SH. Gene expression and dosage: distinct mechanisms regulate benzoate degradation in Acinetobacter baylyi ADP1. [Doctoral Dissertation]. University of Georgia; 2009. Available from: http://purl.galileo.usg.edu/uga_etd/craven_sarah_h_200908_phd

Queens University

2. Garand, Mathieu. Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor .

Degree: Biochemistry, 2010, Queens University

URL: http://hdl.handle.net/1974/5522

► Disequilibrium between coagulation and fibrinolysis can lead to severe haemostatic disorders such as thrombosis and hemophilia. Thrombin-activable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like pro-enzyme… (more)

▼ Disequilibrium between coagulation and fibrinolysis can lead to severe haemostatic disorders such as thrombosis and hemophilia. Thrombin-activable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like pro-enzyme that, once activated, attenuates fibrinolysis. TAFI may also mediate connections between coagulation and inflammation. Studies have associated high plasma TAFI levels with risk for thrombotic diseases. Interestingly, steroid hormones, such as estrogen and progestogens used in hormone replacement therapy or oral contraceptive preparations, have been shown to affect plasma TAFI levels. Regulation of the expression of the gene encoding TAFI, CBP2, is likely an important determinant of the role of the TAFI pathway in vivo; this concept motivated the investigations described in this thesis. In Chapter 2, the results of my research lead to the identification of key transcription factors regulating CPB2. Specifically, we described the binding of NF-Y and HNF-1 to the CPB2 promoter. NF-Y was shown to be an important factor for the basal CPB2 promoter activity. Binding of HNF-1 is essential for the activity of the promoter and is potentially responsible for the liver specific expression of CPB2. In Chapter 3, we set to investigate the effect of female sex hormone on hepatic expression of CPB2. We demonstrated that the levels of TAFI protein secreted from cultured hepatoma cells (HepG2) are decreased by 17beta-estradiol and progesterone. The change in protein expression was paralleled by decreases in CPB2 mRNA abundance and promoter activity. Deletion analysis of the CPB2 promoter indicated that the genomic effects of estrogen and progesterone are likely mediated via a non-classical mechanism. In Chapter 4, we evaluated the effects of various inflammatory mediators on expression of the gene encoding mouse TAFI (Cpb2). Our results showed that Cpb2 mRNA abundance and promoter activity are up-regulated by inflammatory mediators IL-1beta, IL-6, and TNFalpha. We also showed that TNFalpha mediates its effect via the binding of NFkB. Additionally, our results suggest that TNFalpha promotes the binding of NFkB to the promoter by increasing its translocation to the nucleus. The NFkB site is not conserved between human and mouse and may explained the different responses to inflammation observed in vivo.

Subjects/Keywords: Gene; Regulation

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APA (6^th Edition):

Garand, M. (2010). Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/5522

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Garand, Mathieu. “Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor .” 2010. Thesis, Queens University. Accessed July 16, 2019. http://hdl.handle.net/1974/5522.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Garand, Mathieu. “Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor .” 2010. Web. 16 Jul 2019.

Vancouver:

Garand M. Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor . [Internet] [Thesis]. Queens University; 2010. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1974/5522.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Garand M. Regulation of the Gene Encoding Thrombin-Activable Fibrinolysis Inhibitor . [Thesis]. Queens University; 2010. Available from: http://hdl.handle.net/1974/5522

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University

3. Benton, Mary Lauren. Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function.

Degree: MS, Biomedical Informatics, 2018, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-08212018-210357/ ;

► Non-coding gene regulatory enhancers are essential to transcription in mammalian cells. As a result, a large variety of experimental and computational strategies have been developed… (more)

Subjects/Keywords: gene regulation

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APA (6^th Edition):

Benton, M. L. (2018). Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function. (Masters Thesis). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-08212018-210357/ ;

Chicago Manual of Style (16^th Edition):

Benton, Mary Lauren. “Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function.” 2018. Masters Thesis, Vanderbilt University. Accessed July 16, 2019. http://etd.library.vanderbilt.edu/available/etd-08212018-210357/ ;.

MLA Handbook (7^th Edition):

Benton, Mary Lauren. “Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function.” 2018. Web. 16 Jul 2019.

Vancouver:

Benton ML. Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function. [Internet] [Masters thesis]. Vanderbilt University; 2018. [cited 2019 Jul 16]. Available from: http://etd.library.vanderbilt.edu/available/etd-08212018-210357/ ;.

Council of Science Editors:

Benton ML. Genome-wide Enhancer Maps Differ Significantly in their Genomic Distribution, Evolution, and Function. [Masters Thesis]. Vanderbilt University; 2018. Available from: http://etd.library.vanderbilt.edu/available/etd-08212018-210357/ ;

University of Illinois – Urbana-Champaign

4. Chen, Chieh-Chun. Analysis of combinatorial gene regulation with thermodynamic models.

Degree: MS, 0408, 2010, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/14656

► Transcriptional control is a key regulatory mechanism for cells to direct their destinies. A large number of transcription factors (TFs) could simultaneously bind to a… (more)

Subjects/Keywords: Gene Regulation; Gene Regulatory Network

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APA (6^th Edition):

Chen, C. (2010). Analysis of combinatorial gene regulation with thermodynamic models. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/14656

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chen, Chieh-Chun. “Analysis of combinatorial gene regulation with thermodynamic models.” 2010. Thesis, University of Illinois – Urbana-Champaign. Accessed July 16, 2019. http://hdl.handle.net/2142/14656.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chen, Chieh-Chun. “Analysis of combinatorial gene regulation with thermodynamic models.” 2010. Web. 16 Jul 2019.

Vancouver:

Chen C. Analysis of combinatorial gene regulation with thermodynamic models. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2010. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/2142/14656.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chen C. Analysis of combinatorial gene regulation with thermodynamic models. [Thesis]. University of Illinois – Urbana-Champaign; 2010. Available from: http://hdl.handle.net/2142/14656

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

5. Morrissey, Chris S. Understanding the epigenetics of erythroid differentiation through the power of deep sequencing.

Degree: PhD, Integrative Biosciences, 2013, Penn State University

URL: https://etda.libraries.psu.edu/catalog/19905

► Next generation sequencing, or high throughput sequencing, is just over a decade old. In that time the technologies have changed so rapidly that sequencing has… (more)

▼ Next generation sequencing, or high throughput sequencing, is just over a decade old. In that time the technologies have changed so rapidly that sequencing has been surpassing Moore’s Law in that sequencing capacity has been doubling in less than the 18 month pace at which computing power has been doubling since the late 1950s. This prodigious increase in the ability to sequence DNA fragments coupled with the precipitous drop in price has lead to an explosion of the number and type of biological experiments possible. In the ten years since the mouse genome was first sequenced we have gone from being able to detect sequence feature like open reading frames, to being able to compare multiple species revealing differing patterns of evolutionary constraint, to being able to determine the genomic distribution of a whole host of epigenetic features such as histone modifications and DNA bound transcription factors, to being able to sequence cDNA reflections of transcripts. In this dissertation I lay out a strategy for efficiently analyzing and interpreting the mountains of data resulting from modern sequencing experiments. I discuss the software tools used to process sequencing data, and touch on the important runtime parameters. I provide uniform analysis workflows for transcription factor and histone modification ChIP-seq experiments which I have personally used to process data from 55 sequencing experiments. I go on to discuss some of the potential pitfalls that should be avoided, and I provide a blacklist that can be used to filter artifacts from ChIP-seq results. When a transcription factor ChIP-seq experiment is performed, the desired product is a list of genomic locations bound by the transcription factor of interest. To obtain this list, we turn to peak-calling software that interprets the pileup of sequencing reads to determine peak locations. Unfortunately the resulting peaks are very dependent on the peak-calling threshold and other parameters not all of which are well understood. I explore the inherent reproducibility of peak calling in ChIP-seq experiments, and through a combination of sub-sampling and vote counting strive to improve our understanding of peak quality and reproducibility. Finally, I integrate the fruits of my sequencing analysis to illuminate the epigenetics of erythroid differentiation. The Hardison lab utilizes the G1E(Weiss, Yu, & Orkin, 1997) cell line as a model of murine erythropoeisis. G1E cells are an erythroid committed Gata1 knockout cell line derived from mouse embryonic stem cells. GATA1 is a master regulator for erythropoeisis, and without it the G1E cells are stuck in a self renewing erythroid progenitor stage. G1E-ER4 is a GATA1 rescue subline of G1E in which GATA1 can be induced, and differentiation toward erythrocytes can be restored. This is a beautiful system for studying the cascade of differential processes set in motion by the action of this master regulator. Here I use DNase-seq to identify an unprecedentedly comprehensive set of regulatory genomic regions active during…

Subjects/Keywords: Epigenetic gene regulation

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APA (6^th Edition):

Morrissey, C. S. (2013). Understanding the epigenetics of erythroid differentiation through the power of deep sequencing. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/19905

Chicago Manual of Style (16^th Edition):

Morrissey, Chris S. “Understanding the epigenetics of erythroid differentiation through the power of deep sequencing.” 2013. Doctoral Dissertation, Penn State University. Accessed July 16, 2019. https://etda.libraries.psu.edu/catalog/19905.

MLA Handbook (7^th Edition):

Morrissey, Chris S. “Understanding the epigenetics of erythroid differentiation through the power of deep sequencing.” 2013. Web. 16 Jul 2019.

Vancouver:

Morrissey CS. Understanding the epigenetics of erythroid differentiation through the power of deep sequencing. [Internet] [Doctoral dissertation]. Penn State University; 2013. [cited 2019 Jul 16]. Available from: https://etda.libraries.psu.edu/catalog/19905.

Council of Science Editors:

Morrissey CS. Understanding the epigenetics of erythroid differentiation through the power of deep sequencing. [Doctoral Dissertation]. Penn State University; 2013. Available from: https://etda.libraries.psu.edu/catalog/19905

Vanderbilt University

6. Broeckelmann, Eva Marie. Dynamics of long-range gene regulation at the BMP2 locus.

Degree: MS, Interdisciplinary Studies: Human Genetics, 2013, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-04092013-235114/ ;

► A member of the TGF-Ã¢ superfamily of cytokines, BMP2 not only plays a critical role in pattern formation and morphogenesis during early embryonic development, but… (more)

Subjects/Keywords: gene regulation; Bmp2

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APA (6^th Edition):

Broeckelmann, E. M. (2013). Dynamics of long-range gene regulation at the BMP2 locus. (Masters Thesis). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-04092013-235114/ ;

Chicago Manual of Style (16^th Edition):

Broeckelmann, Eva Marie. “Dynamics of long-range gene regulation at the BMP2 locus.” 2013. Masters Thesis, Vanderbilt University. Accessed July 16, 2019. http://etd.library.vanderbilt.edu/available/etd-04092013-235114/ ;.

MLA Handbook (7^th Edition):

Broeckelmann, Eva Marie. “Dynamics of long-range gene regulation at the BMP2 locus.” 2013. Web. 16 Jul 2019.

Vancouver:

Broeckelmann EM. Dynamics of long-range gene regulation at the BMP2 locus. [Internet] [Masters thesis]. Vanderbilt University; 2013. [cited 2019 Jul 16]. Available from: http://etd.library.vanderbilt.edu/available/etd-04092013-235114/ ;.

Council of Science Editors:

Broeckelmann EM. Dynamics of long-range gene regulation at the BMP2 locus. [Masters Thesis]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-04092013-235114/ ;

Rice University

7. Narula, Jatin. Design Principles of Cellular Differentiation Regulatory Networks.

Degree: PhD, Engineering, 2015, Rice University

URL: http://hdl.handle.net/1911/88375

► To understand cellular differentiation programs is to understand the often large and complex gene regulatory networks (GRNs) that control and orchestrate these programs. The work… (more)

▼ To understand cellular differentiation programs is to understand the often large and complex gene regulatory networks (GRNs) that control and orchestrate these programs. The work presented here aims to exploit the wealth of newly available experimental information and methods to identify design principles that relate how GRN structures relate to the functional requirements in three model differentiation/stress-response programs: embryonic hematopoiesis, sporulation and σB general stress response. First we used a statistical thermodynamic approach to characterize the biophysical mechanisms of combinatorial regulation by distant enhancers in eukaryotes and demonstrate how the GRN controlling embryonic hematopoiesis acts as an irreversible bistable switch with low-pass noise filtering properties. We further used our model of the hematopoiesis network to reconcile discrepant experimental observations about the regulator Runx1 and explained how it limits HSC emergence in vitro. In the second project we investigated the Bacillus subtilis sporulation network and showed how a cascade of feed-forward loops downstream of the master regulatory Spo0A~P control cell-fate during starvation. We also identified a rate-responsive network module in the Spo0A regulon to explain why accelerated accumulation of Spo0A~P leads to a dramatic reduction in sporulation efficiency. Further we found that the arrangement of two sporulation network genes on opposite ends of the chromosome ties Spo0A~P activation to the DNA replication status. We were also able to show that the slowdown of cell growth is the primary starvation signal that determines sporulation cell-fates by controlling Spo0A~P activation. For the third project we built a detailed model of the σB network in Bacillus subtilis to mechanistically explain the experimentally observed pulsatile response of this network under stress. We further showed that the same network architecture that enables this pulsatile response insulates the σB network from the effects of competition for cellular resources like RNA polymerase. The design principles identified in the studies of these networks are related to their topological structure and function rather than the specific genes and proteins that comprise them. As a result, we expect them to be widely applicable to and help in the study of a diverse array of other differentiation GRNs. Advisors/Committee Members: Igoshin, Oleg A (advisor), Tabor, Jeffrey J (committee member), Bennett, Matthew R (committee member).

Subjects/Keywords: Differentiation; Gene Regulation

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APA (6^th Edition):

Narula, J. (2015). Design Principles of Cellular Differentiation Regulatory Networks. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/88375

Chicago Manual of Style (16^th Edition):

Narula, Jatin. “Design Principles of Cellular Differentiation Regulatory Networks.” 2015. Doctoral Dissertation, Rice University. Accessed July 16, 2019. http://hdl.handle.net/1911/88375.

MLA Handbook (7^th Edition):

Narula, Jatin. “Design Principles of Cellular Differentiation Regulatory Networks.” 2015. Web. 16 Jul 2019.

Vancouver:

Narula J. Design Principles of Cellular Differentiation Regulatory Networks. [Internet] [Doctoral dissertation]. Rice University; 2015. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1911/88375.

Council of Science Editors:

Narula J. Design Principles of Cellular Differentiation Regulatory Networks. [Doctoral Dissertation]. Rice University; 2015. Available from: http://hdl.handle.net/1911/88375

Washington University in St. Louis

8. Fiore, Christopher Michael. Functional Identification and Characterization of cis-Regulatory Elements.

Degree: PhD, Biology & Biomedical Sciences (Computational & Systems Biology), 2015, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/579

► Transcription is regulated through interactions between regulatory proteins, such as transcription factors (TFs), and DNA sequence. It is known that TFs act combinatorially in… (more)

▼ Transcription is regulated through interactions between regulatory proteins, such as transcription factors (TFs), and DNA sequence. It is known that TFs act combinatorially in some cases to regulate transcription, but in which situations and to what degree is unclear. I first studied the contribution of TF binding sites to expression in mouse embryonic stem (ES) cells by using synthetic cis-regulatory elements (CREs). The synthetic CREs were comprised of combinations of binding sites for the pluripotency TFs Oct4, Sox2, Klf4, and Esrrb. A statistical thermodynamic model explained 72% of the variation in expression driven by these CREs. The high predictive power of this model depended on five TF interaction parameters, including favorable heterotypic interactions between Oct4 and Sox2, Klf4 and Sox2, and Klf4 and Esrrb. The model also included two unfavorable homotypic interaction parameters. These homotypic parameters help to explain the fact that synthetic CREs with mixtures of binding sites for various TFs drive much higher expression than multiple binding sites for the same TF. I then found that the expression of these synthetic CREs largely changes as ES cells differentiate down the neural lineage. However, CREs with no repeat binding sites drove similar levels of expression, suggesting that heterotypic interactions may be similar in the two conditions. In a separate set of experiments I interrogated the determinants of expression driven by genomic sequences previously segmented into classes based on chromatin features. A set of these sequences was assayed in K562 cells. As expected, we found that Enhancers and Weak Enhancers drove expression over background, while Repressed elements and Enhancers from another cell type did not. Unexpectedly, we found that Weak Enhancers drove higher expression than Enhancers, possibly based on their lower H3K36me3 and H3K27ac, which we found to be weakly associated with lower expression. Using a logistic regression model, we showed that matches to TF binding motifs were best able to predict active sequences, but chromatin features contributed significantly as well. These results demonstrate that interactions between certain combinations of pluripotency TFs, but not all combinations, are important to transcriptional regulation. Furthermore, chromatin modifications can still contribute to predictions of expression even after accounting for binding site motifs. Better understanding of the process of cis-regulation will allow us to predict which sequences can drive expression and how perturbations affect this expression. Advisors/Committee Members: Barak A Cohen, Gary Stormo, Justin Fay, Joe Dougherty, Andrew Yoo.

Subjects/Keywords: cis-regulation, Gene Regulation, Regulatory Genomics; Biology

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APA (6^th Edition):

Fiore, C. M. (2015). Functional Identification and Characterization of cis-Regulatory Elements. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/579

Chicago Manual of Style (16^th Edition):

Fiore, Christopher Michael. “Functional Identification and Characterization of cis-Regulatory Elements.” 2015. Doctoral Dissertation, Washington University in St. Louis. Accessed July 16, 2019. https://openscholarship.wustl.edu/art_sci_etds/579.

MLA Handbook (7^th Edition):

Fiore, Christopher Michael. “Functional Identification and Characterization of cis-Regulatory Elements.” 2015. Web. 16 Jul 2019.

Vancouver:

Fiore CM. Functional Identification and Characterization of cis-Regulatory Elements. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2015. [cited 2019 Jul 16]. Available from: https://openscholarship.wustl.edu/art_sci_etds/579.

Council of Science Editors:

Fiore CM. Functional Identification and Characterization of cis-Regulatory Elements. [Doctoral Dissertation]. Washington University in St. Louis; 2015. Available from: https://openscholarship.wustl.edu/art_sci_etds/579

University of Saskatchewan

9. Narayanan, Karthikeyan. SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE.

Degree: 2014, University of Saskatchewan

URL: http://hdl.handle.net/10388/ETD-2014-06-1601

► Carotenoids are organic pigments that are mainly found in the chloroplasts and chromoplasts of plants and other photosynthetic organisms. Carotenoid molecules containing oxygen, such as… (more)

▼ Carotenoids are organic pigments that are mainly found in the chloroplasts and chromoplasts of plants and other photosynthetic organisms. Carotenoid molecules containing oxygen, such as lutein, violaxanthin and zeaxanthin are called xanthophylls and the rest containing un-oxygenated carotenoids are known as carotenes. Carotenoids form the integral part of the photosystem II LHC. Xanthophylls mainly aid in light harvesting and dissipation of harmful excess energy from excited chlorophyll molecules, thereby protecting chlorophyll from photo-degradation. The biosynthesis of carotenoids has been widely studied using plant and algae. However, the regulatory mechanisms involved in carotenoid metabolism need better understanding. This thesis identified novel regulatory mechanisms involved in the carotenoid biosynthetic pathway using activation-tagged Arabidopsis mutants. Two screening methods, red seed coat screening and norflurazon resistance screening, were used in this study. Fourteen mutants were screened using red seed coat screening but a successful mutant characterization could not be performed due to the unavailability of mutants with a single copy T-DNA insertion. Norflurazon screening identified eight mutants, out of which two mutants, KN203 and KN231, were characterized. The KN203 mutant had a defective keto-acyl CoA synthase 19 gene. KN203 mutant had lower carotenoid levels in the leaves and increased carotenoid levels in the mature seeds; the mutant was able to revert back to wild type phenotype after complementation of a functional KCS19 gene copy driven by native promoter. The fatty acid analysis indicated that the mutant KN203 had decreased MGDG and increased lysoPG, lysoPC and lysoPE content. Reduced carotenoid content in KN203 leaves was attributed to changes in fatty acid composition of chloroplast envelope membrane. Mutant KN231 had a T-DNA insertion in a gene encoding a RNA binding protein (RBP47C). KN231 leaf carotenoid levels were similar to wild type but their levels were significantly higher in their seeds. Two allelic mutants were selected to characterize the mutants. Overexpression of functional RBP47C in the mutants reverted to wild type phenotype in some overexpression mutants. A tandem repeat homologue of RBP47C, RBP47C’was identified. In-silico analysis predicted RBP47C to be a potential candidate for chloroplast localization. Advisors/Committee Members: Khachatourians, George, Gruber, Margie, Hegedus, Dwayne, Gray, Gordon, Qiu, Xiao.

Subjects/Keywords: Carotneoids; RBP47; KCS19; Gene expression; Gene regulation

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APA (6^th Edition):

Narayanan, K. (2014). SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/ETD-2014-06-1601

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Narayanan, Karthikeyan. “SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE.” 2014. Thesis, University of Saskatchewan. Accessed July 16, 2019. http://hdl.handle.net/10388/ETD-2014-06-1601.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Narayanan, Karthikeyan. “SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE.” 2014. Web. 16 Jul 2019.

Vancouver:

Narayanan K. SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE. [Internet] [Thesis]. University of Saskatchewan; 2014. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/10388/ETD-2014-06-1601.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Narayanan K. SCREENING AND CHARACTERIZATION OF ARABIDOPSIS THALIANA MUTANTS WITH ALTERED CAROTENOID PROFILE. [Thesis]. University of Saskatchewan; 2014. Available from: http://hdl.handle.net/10388/ETD-2014-06-1601

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

10. Alasoo, Kaur. Regulation of gene expression in macrophage immune response .

Degree: 2017, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/263855

► Gene expression quantitative trait loci (eQTL) mapping studies can provide mechanistic insights into the functions of disease-associated variants. However, many eQTLs are cell type and… (more)

▼ Gene expression quantitative trait loci (eQTL) mapping studies can provide mechanistic insights into the functions of disease-associated variants. However, many eQTLs are cell type and context specific. This is particularly relevant for immune cells, whose cellular function and behaviour can be substantially altered by external cues. Furthermore, understanding mechanisms behind eQTLs is hindered by the difficulty of identifying causal variants. We differentiated macrophages from induced pluripotent stem cells from 86 unrelated, healthy individuals derived as part of the Human Induced Pluripotent Stem Cells Initiative. We generated RNA-seq data from these cells in four experimental conditions: naïve, interferon- gamma (IFNɣ) treatment (18h), Salmonella infection (5h), and IFNγ treatment followed by Salmonella infection. We also measured chromatin accessibility with ATAC-seq in 31-42 individuals in the same four conditions. We detected gene expression QTLs (eQTLs) for 4326 genes, over 900 of which were condition-specific. We also detected a similar number of transcript ratio QTLs (trQTLs) that influenced mRNA processing and alternative splicing. Macrophage eQTLs and trQTLs were enriched for variants associated with Alzheimer’s disease, multiple autoimmune disorders and lipid traits. We also detected chromatin accessibility QTLs (caQTLs) for 14,602 accessible regions, including hundreds of long-range interactions. Joint analysis of eQTLs with caQTLs allowed us to greatly reduce the set of credible causal variants, often pinpointing to a single most likely variant. We found that caQTLs were less condition- specific than eQTLs and ~50% of the stimulation-specific eQTLs manifested on the chromatin level already in the naive cells. These observations might help to explain the discrepancy between strong enrichment of diseases associations in regulatory elements but only modest overlap with current eQTL studies, suggesting that many regulatory elements are in a ‘primed’ state waiting for an appropriate environmental signal before regulating gene expression.

Subjects/Keywords: Gene expression; Gene regulation; Chromatin; Genetics

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Alasoo, K. (2017). Regulation of gene expression in macrophage immune response . (Thesis). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/263855

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Alasoo, Kaur. “Regulation of gene expression in macrophage immune response .” 2017. Thesis, University of Cambridge. Accessed July 16, 2019. https://www.repository.cam.ac.uk/handle/1810/263855.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Alasoo, Kaur. “Regulation of gene expression in macrophage immune response .” 2017. Web. 16 Jul 2019.

Vancouver:

Alasoo K. Regulation of gene expression in macrophage immune response . [Internet] [Thesis]. University of Cambridge; 2017. [cited 2019 Jul 16]. Available from: https://www.repository.cam.ac.uk/handle/1810/263855.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Alasoo K. Regulation of gene expression in macrophage immune response . [Thesis]. University of Cambridge; 2017. Available from: https://www.repository.cam.ac.uk/handle/1810/263855

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

11. Alasoo, Kaur. Regulation of gene expression in macrophage immune response.

Degree: PhD, 2017, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/263855 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715945

► Gene expression quantitative trait loci (eQTL) mapping studies can provide mechanistic insights into the functions of disease-associated variants. However, many eQTLs are cell type and… (more)

▼ Gene expression quantitative trait loci (eQTL) mapping studies can provide mechanistic insights into the functions of disease-associated variants. However, many eQTLs are cell type and context specific. This is particularly relevant for immune cells, whose cellular function and behaviour can be substantially altered by external cues. Furthermore, understanding mechanisms behind eQTLs is hindered by the difficulty of identifying causal variants. We differentiated macrophages from induced pluripotent stem cells from 86 unrelated, healthy individuals derived as part of the Human Induced Pluripotent Stem Cells Initiative. We generated RNA-seq data from these cells in four experimental conditions: naïve, interferon- gamma (IFNɣ) treatment (18h), Salmonella infection (5h), and IFNγ treatment followed by Salmonella infection. We also measured chromatin accessibility with ATAC-seq in 31-42 individuals in the same four conditions. We detected gene expression QTLs (eQTLs) for 4326 genes, over 900 of which were condition-specific. We also detected a similar number of transcript ratio QTLs (trQTLs) that influenced mRNA processing and alternative splicing. Macrophage eQTLs and trQTLs were enriched for variants associated with Alzheimer’s disease, multiple autoimmune disorders and lipid traits. We also detected chromatin accessibility QTLs (caQTLs) for 14,602 accessible regions, including hundreds of long-range interactions. Joint analysis of eQTLs with caQTLs allowed us to greatly reduce the set of credible causal variants, often pinpointing to a single most likely variant. We found that caQTLs were less condition- specific than eQTLs and ~50% of the stimulation-specific eQTLs manifested on the chromatin level already in the naive cells. These observations might help to explain the discrepancy between strong enrichment of diseases associations in regulatory elements but only modest overlap with current eQTL studies, suggesting that many regulatory elements are in a ‘primed’ state waiting for an appropriate environmental signal before regulating gene expression.

Subjects/Keywords: 616.07; Gene expression; Gene regulation; Chromatin; Genetics

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Alasoo, K. (2017). Regulation of gene expression in macrophage immune response. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/263855 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715945

Chicago Manual of Style (16^th Edition):

Alasoo, Kaur. “Regulation of gene expression in macrophage immune response.” 2017. Doctoral Dissertation, University of Cambridge. Accessed July 16, 2019. https://www.repository.cam.ac.uk/handle/1810/263855 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715945.

MLA Handbook (7^th Edition):

Alasoo, Kaur. “Regulation of gene expression in macrophage immune response.” 2017. Web. 16 Jul 2019.

Vancouver:

Alasoo K. Regulation of gene expression in macrophage immune response. [Internet] [Doctoral dissertation]. University of Cambridge; 2017. [cited 2019 Jul 16]. Available from: https://www.repository.cam.ac.uk/handle/1810/263855 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715945.

Council of Science Editors:

Alasoo K. Regulation of gene expression in macrophage immune response. [Doctoral Dissertation]. University of Cambridge; 2017. Available from: https://www.repository.cam.ac.uk/handle/1810/263855 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715945

Texas A&M University

12. Malik, Indranil. In Vivo Consequences of Altered Pol II Catalysis.

Degree: PhD, Biochemistry, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/165890

► Gene transcription by RNA polymerase II (Pol II) is an essential process. Using Saccharomyces cerevisiae as a model system, our lab has previously identified and… (more)

▼ Gene transcription by RNA polymerase II (Pol II) is an essential process. Using Saccharomyces cerevisiae as a model system, our lab has previously identified and partially characterized Pol II activity mutants that can alter catalysis rate to faster or slower than wild type in vitro. In my dissertation research I use a set of these Pol II activity mutants to determine consequences of altered catalysis rate on polymerase functions, co-transcriptional pre-mRNA processing and gene expression in vivo. I show that alteration in Pol II catalytic rate, either increase or decrease, leads to a decreased Pol II occupancy and an apparent reduction in elongation rate on a commonly used reporter gene in vivo. Measurement of in vivo elongation rate on this reporter requires transcriptional shutoff followed by ChIP. I discover that some Pol II catalytic mutants can compromise the kinetics of transcription shutoff by glucose, which is generally assumed to be unaffected by transcription mutants. Further, I show that Pol II catalytic mutants affect model gene expression and the effects on gene expression are exacerbated with increased promoter strength and gene length. My results suggest that gene expression defects in the Pol II mutants may in part result from defective mRNA processing. Additionally, I show that mRNA half-lives for that model gene are increased in Pol II mutant strains and the magnitude of half-life changes correlate both with mutants? growth and the magnitude of reporter gene expression defects. Finally, I test if altered Pol II elongation sensitizes cells to nucleotide depletion and find that Pol II mutants and several elongation factor mutants respond to GTP starvation similarly to wild type and that putative elongation defects are not likely to drive the cellular response to limiting GTP. Altogether my findings reveal wide-ranging in vivo effects of Pol II catalytic mutants, which will be critical for precise use of these Pol II catalytic mutants in gene regulation studies. Advisors/Committee Members: Kaplan, Craig D (advisor), Rye, Hays (committee member), Polymenis, Michael (committee member), Sachs, Matthew S (committee member).

Subjects/Keywords: Transcription; RNA polymerase; Gene regulation

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Malik, I. (2017). In Vivo Consequences of Altered Pol II Catalysis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/165890

Chicago Manual of Style (16^th Edition):

Malik, Indranil. “In Vivo Consequences of Altered Pol II Catalysis.” 2017. Doctoral Dissertation, Texas A&M University. Accessed July 16, 2019. http://hdl.handle.net/1969.1/165890.

MLA Handbook (7^th Edition):

Malik, Indranil. “In Vivo Consequences of Altered Pol II Catalysis.” 2017. Web. 16 Jul 2019.

Vancouver:

Malik I. In Vivo Consequences of Altered Pol II Catalysis. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1969.1/165890.

Council of Science Editors:

Malik I. In Vivo Consequences of Altered Pol II Catalysis. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/165890

University of Tasmania

13. Phillips, JL. Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms.

Degree: 2017, University of Tasmania

URL: https://eprints.utas.edu.au/23900/1/Phillips_whole_thesis.pdf ; Phillips, JL ORCID: 0000-0002-5559-3072 <https://orcid.org/0000-0002-5559-3072> 2017 , 'Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms', PhD thesis, University of Tasmania.

► Disruption to regulatory mechanisms controlling gene expression is a hallmark of leukaemia, with disruption to transcription factors being one of the most prevalent. By identifying… (more)

▼ Disruption to regulatory mechanisms controlling gene expression is a hallmark of leukaemia, with disruption to transcription factors being one of the most prevalent. By identifying the gene expression profile under the control of these transcription factors, and understanding how the target genes are regulated, critical insight can be gained into the role of these transcription factors in haematopoiesis, as well as their role in leukaemia development. Evidence presented here suggests that the RUNX1 transcription factor regulates the expression of the α6β4 integrin receptor in haematopoietic cells by controlling the integrin genes ITGA6 and ITGB4. Engagement of integrin receptors with extracellular matrix components of the bone marrow and haematopoietic tissues plays an essential role in haematopoiesis. Integrin expression is also altered in many leukaemias, however the regulation of integrin gene expression both in normal and disease states has remained largely unexplored. Data presented here identified ITGA6 and ITGB4 as novel target genes of the RUNX1 transcription factor in myeloid cells. RUNX1 was found to bind to the promoter regions of ITGA6 and ITGB4 in myeloid cells in ChIP assays. Furthermore, RUNX1 had a functional effect on both of the promoters in reporter assays. RUNX1 increased the activity of both promoters, while RUNX1-ETO, which is produced by a common chromosomal translocation in leukaemic cells, repressed promoter activity, consistent with its well-characterised role as a transcriptional repressor. While RUNX1 is commonly described as a sequence-specific DNA binding protein that binds to the consensus motif TGT/cGGT, it is becoming evident that the regulation of genes by RUNX1 is more complex than this and RUNX1 can regulate its target genes through a variety of mechanisms. Evidence presented here suggests that RUNX1 regulates the ITGA6 and ITGB4 integrin genes via two distinct mechanisms. RUNX1 was found to regulate the ITGA6 promoter through a consensus RUNX1 binding motif and RUNX1 activation of the promoter was dependent on this motif, in keeping with the traditional model of RUNX1 function described in the literature. In contrast, RUNX1 does not target the ITGB4 promoter through a consensus sequence motif and may be recruited indirectly to the promoter by other haematopoietic transcription factors. Furthermore, the data presented here suggest that efficient regulation of the ITGB4 gene may require interactions between the promoter and an upstream enhancer. RUNX1 was also found to interact with the ITGB4 enhancer, and similarly to the promoter, these interactions do not require a RUNX1 consensus binding motif and may involve recruitment by other transcription factors. Recent evidence suggests that the traditional model of RUNX1 function through a consensus binding motif may represent only a small proportion of RUNX1 target genes. Genome-wide analysis suggests that a significant proportion of RUNX1 recruitment to DNA occurs in the absence of consensus binding motifs, as shown here for ITGB4.…

Subjects/Keywords: gene regulation; integrins; epigenetics RUNX1

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Phillips, J. (2017). Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/23900/1/Phillips_whole_thesis.pdf ; Phillips, JL ORCID: 0000-0002-5559-3072 <https://orcid.org/0000-0002-5559-3072> 2017 , 'Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms', PhD thesis, University of Tasmania.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Phillips, JL. “Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms.” 2017. Thesis, University of Tasmania. Accessed July 16, 2019. https://eprints.utas.edu.au/23900/1/Phillips_whole_thesis.pdf ; Phillips, JL ORCID: 0000-0002-5559-3072 <https://orcid.org/0000-0002-5559-3072> 2017 , 'Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms', PhD thesis, University of Tasmania..

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Phillips, JL. “Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms.” 2017. Web. 16 Jul 2019.

Vancouver:

Phillips J. Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms. [Internet] [Thesis]. University of Tasmania; 2017. [cited 2019 Jul 16]. Available from: https://eprints.utas.edu.au/23900/1/Phillips_whole_thesis.pdf ; Phillips, JL ORCID: 0000-0002-5559-3072 <https://orcid.org/0000-0002-5559-3072> 2017 , 'Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms', PhD thesis, University of Tasmania..

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Phillips J. Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms. [Thesis]. University of Tasmania; 2017. Available from: https://eprints.utas.edu.au/23900/1/Phillips_whole_thesis.pdf ; Phillips, JL ORCID: 0000-0002-5559-3072 <https://orcid.org/0000-0002-5559-3072> 2017 , 'Regulation of ITGA6 and ITGB4 integrin genes by RUNX1 and epigenetic mechanisms', PhD thesis, University of Tasmania.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Tasmania

14. Apps, LD. Regulation of inducible immune gene expression in T cells compared to macrophages.

Degree: 2014, University of Tasmania

URL: https://eprints.utas.edu.au/18558/1/Whole-Apps-thesis.pdf

► The initiation, duration and resolution of an appropriate immune response is vital for defending the host against invading pathogens, toxins and cancerous cells. Such immune… (more)

▼ The initiation, duration and resolution of an appropriate immune response is vital for defending the host against invading pathogens, toxins and cancerous cells. Such immune responses are reliant on the cooperative action of multiple cell types and the co-ordinated regulation of gene expression programs, which direct immune function. Inducible gene expression upon immune activation is determined by the complex interaction between transcription factors, the chromatin structure and chromatin modifying/remodelling factors at the regulatory regions of immune genes. The NF-κB transcription factor c-Rel is a key regulator of gene expression programs within the immune system. c-Rel regulates expression of cytokines and transcription factors during immune cell activation and is essential for the correct function of immune cells from divergent cell lineages. These differentiated cells are highly specialised and have a diverse range of functions requiring precise regulation of their gene expression profiles for targeted responses. This study explores the role of c-Rel in divergent lymphocyte and macrophage lineages. c-Rel has previously been shown to instigate chromatin remodelling events required for activation of the GM-CSF gene in T cells. Activation involves the depletion of hyper-acetylated histones from the promoter region of the gene, mediated by the chromatin remodelling protein BRG1. This study shows that activation of the GM-CSF gene is also c-Rel dependent in macrophages, however the gene promoter is not marked by acetylated chromatin and no loss of H3 is detected in association with activation. These findings suggest that whilst the GM-CSF gene is expressed in both T cells and macrophages, activation is regulated by fundamentally different mechanisms in the two cell types. The hypothesis underlying this study is that during the process of differentiation lineage specific chromatin structure is established at inducible gene promoters and that this chromatin structure largely dictates the cooperative regulation of gene expression through interaction with transcription factors, structural proteins and chromatin remodelling enzymes. Using genome-wide data sets, a cohort of immune genes which are regulated by c-Rel were identified. These genes were further categorised into BRG1 independent and dependent genes. The activation requirements of these genes were examined in both T cells and macrophages to determine whether the switch in regulatory control identified for the GM-CSF gene is a common feature of genes that are co-expressed by these cell types, and to characterise the mechanisms underlying this fundamental difference in regulation. Data presented in this thesis demonstrates that several genes undergo switches in the requirements for gene expression between the two cell types. The analysis of chromatin structure indicates that these differences in activation kinetics are reflective of the basal chromatin accessibility established at the genes promoter regions. Furthermore, the extent of chromatin remodelling…

Subjects/Keywords: Epigenetics; gene regulation; immune response

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Apps, L. (2014). Regulation of inducible immune gene expression in T cells compared to macrophages. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/18558/1/Whole-Apps-thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Apps, LD. “Regulation of inducible immune gene expression in T cells compared to macrophages.” 2014. Thesis, University of Tasmania. Accessed July 16, 2019. https://eprints.utas.edu.au/18558/1/Whole-Apps-thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Apps, LD. “Regulation of inducible immune gene expression in T cells compared to macrophages.” 2014. Web. 16 Jul 2019.

Vancouver:

Apps L. Regulation of inducible immune gene expression in T cells compared to macrophages. [Internet] [Thesis]. University of Tasmania; 2014. [cited 2019 Jul 16]. Available from: https://eprints.utas.edu.au/18558/1/Whole-Apps-thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Apps L. Regulation of inducible immune gene expression in T cells compared to macrophages. [Thesis]. University of Tasmania; 2014. Available from: https://eprints.utas.edu.au/18558/1/Whole-Apps-thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Case Western Reserve University

15. Xu, Xiaohong. SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER.

Degree: PhD, Neurosciences, 2007, Case Western Reserve University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1157660172

► The nicotinic acetylcholine receptor (nAChR) â4, á3, á5 gene cluster encodes several heteromeric transmitter receptor subtypes that are essential for cholinergic synaptic transmission in the… (more)

Subjects/Keywords: transcription regulation gene cluster

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Xu, X. (2007). SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER. (Doctoral Dissertation). Case Western Reserve University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1157660172

Chicago Manual of Style (16^th Edition):

Xu, Xiaohong. “SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER.” 2007. Doctoral Dissertation, Case Western Reserve University. Accessed July 16, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1157660172.

MLA Handbook (7^th Edition):

Xu, Xiaohong. “SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER.” 2007. Web. 16 Jul 2019.

Vancouver:

Xu X. SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER. [Internet] [Doctoral dissertation]. Case Western Reserve University; 2007. [cited 2019 Jul 16]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1157660172.

Council of Science Editors:

Xu X. SHARED LONG-RANGE REGULATORY ELEMENTS COORDINATE EXPRESSION OF THE NACHR BETA4/ALPHA3/ALPHA5 CLUSTER. [Doctoral Dissertation]. Case Western Reserve University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1157660172

Penn State University

16. Missra, Anamika. BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX.

Degree: PhD, Biochemistry, Microbiology, and Molecular Biology, 2010, Penn State University

URL: https://etda.libraries.psu.edu/catalog/10560

► NELF (Negative Elongation Factor) and DSIF (DRB sensitivity inducing factor) are involved in pausing RNA Polymerase II (Pol II) in the promoter proximal region of… (more)

Subjects/Keywords: gene regulation; transcription; polymerase

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Missra, A. (2010). BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/10560

Chicago Manual of Style (16^th Edition):

Missra, Anamika. “BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX.” 2010. Doctoral Dissertation, Penn State University. Accessed July 16, 2019. https://etda.libraries.psu.edu/catalog/10560.

MLA Handbook (7^th Edition):

Missra, Anamika. “BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX.” 2010. Web. 16 Jul 2019.

Vancouver:

Missra A. BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX. [Internet] [Doctoral dissertation]. Penn State University; 2010. [cited 2019 Jul 16]. Available from: https://etda.libraries.psu.edu/catalog/10560.

Council of Science Editors:

Missra A. BIOCHEMICAL ANALYSIS OF INTERACTIONS OF DSIF AND NELF WITH THE DROSOPHILA RNA POLYMERASE II TRANSCRIPTION ELONGATION COMPLEX. [Doctoral Dissertation]. Penn State University; 2010. Available from: https://etda.libraries.psu.edu/catalog/10560

University of Sydney

17. Szyszka, Taylor Nicole. Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 .

Degree: 2019, University of Sydney

URL: http://hdl.handle.net/2123/20221

► The work presented in this Thesis examines aspects of the molecular mechanisms underlying gene regulation, focusing on the bromodomain and extra-terminal domain (BET) protein family.… (more)

Subjects/Keywords: NMR; Protein; Structure; Gene Regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Szyszka, T. N. (2019). Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20221

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Szyszka, Taylor Nicole. “Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 .” 2019. Thesis, University of Sydney. Accessed July 16, 2019. http://hdl.handle.net/2123/20221.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Szyszka, Taylor Nicole. “Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 .” 2019. Web. 16 Jul 2019.

Vancouver:

Szyszka TN. Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 . [Internet] [Thesis]. University of Sydney; 2019. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/2123/20221.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Szyszka TN. Structural Studies of Bromodomain and Extra-Terminal Domain Protein BRD3 . [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/20221

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech

18. Kadelka, Claus Thomas. Robustness Analysis of Gene Regulatory Networks.

Degree: PhD, Mathematics, 2015, Virginia Tech

URL: http://hdl.handle.net/10919/73302

► Cells generally manage to maintain stable phenotypes in the face of widely varying environmental conditions. This fact is particularly surprising since the key step of… (more)

▼ Cells generally manage to maintain stable phenotypes in the face of widely varying environmental conditions. This fact is particularly surprising since the key step of gene expression is fundamentally a stochastic process. Many hypotheses have been suggested to explain this robustness. First, the special topology of gene regulatory networks (GRNs) seems to be an important factor as they possess feedforward loops and certain other topological features much more frequently than expected. Second, genes often regulate each other in a canalizing fashion: there exists a dominance order amidst the regulators of a gene, which in silico leads to very robust phenotypes. Lastly, an entirely novel gene regulatory mechanism, discovered and studied during the last two decades, which is believed to play an important role in cancer, is shedding some light on how canalization may in fact take place as part of a cell’s gene regulatory program. Short segments of single-stranded RNA, so-called microRNAs, which are embedded in several different types of feedforward loops, help smooth out noise and generate canalizing effects in gene regulation by overriding the effect of certain genes on others. Boolean networks and their multi-state extensions have been successfully used to model GRNs for many years. In this dissertation, GRNs are represented in the time- and statediscrete framework of Stochastic Discrete Dynamical Systems (SDDS), which captures the cell-inherent stochasticity. Each gene has finitely many different concentration levels and its concentration at the next time step is determined by a gene-specific update rule that depends on the current concentration of the gene’s regulators. The update rules in published gene regulatory networks are often nested canalizing functions. In Chapter 2, this class of functions is introduced, generalized and analyzed with respect to its potential to confer robustness. Chapter 3 describes a simulation study, which supports the hypothesis that microRNA-mediated feedforward loops have a stabilizing effect on GRNs. Chapter 4 focuses on the cellular DNA mismatch repair machinery. A first regulatory network for this machinery is introduced, partly validated and analyzed with regard to the role of microRNAs and certain genes in conferring robustness to this particular network. Due to steady exposure to mutations, GRNs have evolved over time into their current form. In Chapter 5, a new framework for modeling the evolution of GRNs is developed and then used to identify topological features that seem to stabilize GRNs on an evolutionary time-scale. Chapter 6 addresses a completely separate project in Bioinformatics. A novel functional enrichment method is developed and compared to various popular methods. Funding for this work was provided by NSF grant CMMI-0908201 and NSF grant 1062878. Advisors/Committee Members: Laubenbacher, Reinhard C. (committeechair), Herdman, Terry L. (committee member), Murali, T M. (committee member), Ciupe, Mihaela Stanca (committee member).

Subjects/Keywords: Boolean network; gene regulation; stability

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kadelka, C. T. (2015). Robustness Analysis of Gene Regulatory Networks. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/73302

Chicago Manual of Style (16^th Edition):

Kadelka, Claus Thomas. “Robustness Analysis of Gene Regulatory Networks.” 2015. Doctoral Dissertation, Virginia Tech. Accessed July 16, 2019. http://hdl.handle.net/10919/73302.

MLA Handbook (7^th Edition):

Kadelka, Claus Thomas. “Robustness Analysis of Gene Regulatory Networks.” 2015. Web. 16 Jul 2019.

Vancouver:

Kadelka CT. Robustness Analysis of Gene Regulatory Networks. [Internet] [Doctoral dissertation]. Virginia Tech; 2015. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/10919/73302.

Council of Science Editors:

Kadelka CT. Robustness Analysis of Gene Regulatory Networks. [Doctoral Dissertation]. Virginia Tech; 2015. Available from: http://hdl.handle.net/10919/73302

University of Adelaide

19. Raimondo, Anne. Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1.

Degree: 2011, University of Adelaide

URL: http://hdl.handle.net/2440/73199

► Single-minded 1 (SIM1) is a basic Helix-Loop-Helix/PER-ARNT-SIM (bHLH/PAS) transcription factor essential for survival in mice. The early post-natal lethality exhibited by Sim1⁻ʹ⁻ mice is believed… (more)

▼ Single-minded 1 (SIM1) is a basic Helix-Loop-Helix/PER-ARNT-SIM (bHLH/PAS) transcription factor essential for survival in mice. The early post-natal lethality exhibited by Sim1⁻ʹ⁻ mice is believed to be the consequence of severely compromised hypothalamus development, although the contribution of reduced SIM1 signalling in the numerous other tissues in which it is expressed has never been formally investigated. The presence of a single Sim1 allele is sufficient to avoid this perinatal lethality, and instead confers an early onset, hyperphagic obesity phenotype, potentially via disruption of critical intracellular signalling pathways that are activated in Sim1-expressing hypothalamic neurons in response to food intake. Similar correlations between reduced SIM1 gene dosage and severe obesity have also been documented in humans. Alterations in SIM1 expression and/or function therefore have important implications in health and disease, and warrant a detailed investigation into the downstream target genes and regulatory behaviours of this critical transcription factor, which are thus far almost entirely lacking in the literature. The studies presented in this thesis describe a twofold approach to dissecting the gene regulatory properties of the SIM1 protein. Firstly, we optimised and performed a range of functional assays, including a cell-based luciferase reporter gene assay, a subcellular localisation assay, a co-immunoprecipitation assay, and an electrophoretic mobility shift assay, which were designed to assess the contribution of nineteen unique point mutations within the SIM1 protein sequence to altered SIM1 expression and behaviour. These nineteen mutations were identified in multiple cohorts of severely obese humans, and therefore represent potentially pathogenic alterations in the SIM1 sequence. Indeed, we observed a significant loss of function for many of these variants in luciferase reporter gene assays relative to wild type SIM1. The severe loss of function observed for one of these variants, SIM1 T292A, could be further attributed to altered subcellular localisation, thus impacting on its ability to form a stable heterodimer with ARNT2 in co-immunoprecipitation experiments. Secondly, we performed microarray studies on cultured kidney-derived cells inducibly overexpressing Myc-tagged SIM1 and its obligate partner factor ARNT2, and subsequently identified several genes that selectively responded to SIM/ARNT2 overexpression in this context. Further validation in hypothalamus-derived cultured cells highlighted Myomesin 2 (Myom2) as a potentially genuine downstream SIM1 target gene in both kidney and hypothalamus. We also present data that are the first to indicate Somatostatin (Ss) as a hypothalamic target gene regulated by SIM1 in a cell-autonomous manner. These data are among the first to dissect the downstream target genes and regulatory properties of the SIM1 protein, and therefore make an important contribution to our understanding of the molecular basis to the hyperphagic obesity exhibited by Sim1⁺ʹ⁻ mice.… Advisors/Committee Members: Whitelaw, Murray Leslie (advisor), Chapman-Smith, Anne (advisor), Koblar, Simon Andrea (advisor), School of Molecular and Biomedical Science (school).

Subjects/Keywords: transcription; gene regulation; obesity

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APA (6^th Edition):

Raimondo, A. (2011). Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/73199

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Raimondo, Anne. “Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1.” 2011. Thesis, University of Adelaide. Accessed July 16, 2019. http://hdl.handle.net/2440/73199.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Raimondo, Anne. “Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1.” 2011. Web. 16 Jul 2019.

Vancouver:

Raimondo A. Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1. [Internet] [Thesis]. University of Adelaide; 2011. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/2440/73199.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Raimondo A. Identification of downstream target genes and analysis of obesity-related variants of the bHLH/PAS transcription factor single-minded 1. [Thesis]. University of Adelaide; 2011. Available from: http://hdl.handle.net/2440/73199

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Cornell University

20. Wissink, Erin. Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements .

Degree: 2016, Cornell University

URL: http://hdl.handle.net/1813/43605

► Post-transcriptional events control the amount of protein produced by an mRNA transcript. In mammals, the sequences that regulate post-transcriptional events are predominantly located within a… (more)

▼ Post-transcriptional events control the amount of protein produced by an mRNA transcript. In mammals, the sequences that regulate post-transcriptional events are predominantly located within a transcript's 3′ untranslated region (UTR), and these cisregulatory elements alter rates of mRNA decay and translation via interactions with trans-factors, including microRNAs and RNA binding proteins. It is challenging to identify the sequences within 3′ UTRs that have regulatory function and to determine the importance of cis-regulatory elements to cellular phenotypes. In this work, I discovered hundreds of functional sequences within 3′ UTRs by creating a fluorescence-based reporter assay that tested in parallel thousands of possible small sequences' regulatory potential. These functional sequences included both elements able to increase and to decrease expression of the reporter gene, demonstrating that 3′ UTRs can have activating and repressive roles. Importantly, sequences discovered from this screen were able to regulate expression of endogenous 3′ UTRs. Smaller sub-motifs are enriched within activating and repressive elements, suggesting that sequences 3-5 nucleotides in length can confer post-transcriptional regulation. The novel cis-regulatory elements discovered in this screen will greatly increase our understanding of how mRNA transcripts and their translation are regulated. Additionally, I examined the role of microRNAs in CD8+ T cells, which allowed me to investigate how cis-regulatory elements can affect the adaptive immune system. CD8+ T cells are responsible for recognizing and killing cells that have been infected with intracellular pathogens, and they require miRNAs, a class of post-transcriptional trans-factors, in order to reach sites of infection and kill cells efficiently. I found that a specific microRNA, miR-150, is highly expressed in CD8+ T cells, and in its absence, CD8+ T cells have widespread misregulation of genes, including a failure to produce genes needed for proliferation and response to infection. I also identified microRNAs that are differentially expressed in adult and neonatal CD8+ T cells, and these microRNAs may underlie the inability of neonatal cells to survive an infection. The targets of two differentially expressed miRNAs, miR-29 and miR-130, are themselves differentially expressed in neonatal CD8+ T cells. These results demonstrate that posttranscriptional events are required for CD8+ T cells to correctly respond to infection. Advisors/Committee Members: Lis,John T. (committeeMember), Rudd,Brian D. (committeeMember), Soloway,Paul (committeeMember).

Subjects/Keywords: gene regulation; immunology; development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wissink, E. (2016). Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/43605

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wissink, Erin. “Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements .” 2016. Thesis, Cornell University. Accessed July 16, 2019. http://hdl.handle.net/1813/43605.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wissink, Erin. “Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements .” 2016. Web. 16 Jul 2019.

Vancouver:

Wissink E. Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements . [Internet] [Thesis]. Cornell University; 2016. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1813/43605.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wissink E. Post-Transcriptional Gene Regulation: Roles For Micrornas In Cd8+ T Cells And Discovery Of Novel Cis-Regulatory Elements . [Thesis]. Cornell University; 2016. Available from: http://hdl.handle.net/1813/43605

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Edinburgh

21. Buckle, Adam James. Regulatory architecture of the Pax6 locus.

Degree: PhD, 2014, University of Edinburgh

URL: http://hdl.handle.net/1842/16878

► Pax6 is a highly conserved developmental regulator with a complex temporal, spatial and quantitative expression pattern, that is crucial for correct development of the central… (more)

▼ Pax6 is a highly conserved developmental regulator with a complex temporal, spatial and quantitative expression pattern, that is crucial for correct development of the central nervous system, the eye, and pancreas. Accordingly, the Pax6 gene resides in a complex genomic locus containing a large array of long-range tissue-specific cis-regulatory elements primarily identified through multispecies sequence conservation and reporter studies. I have set out to understand how the chromatin architecture of the locus contributes to the mechanism and specificity of cis-regulatory interactions. As well as addressing whether the DNA looping model for regulatory interactions applies to the mouse Pax6 locus, I will identify which elements facilitate such interactions and if they vary between cell types. Utilising ChIP-array technology the distribution and variability of key regulatory histone modifications and factors were assessed in a set of Pax6 expressing and non-expressing mouse cell lines, acting as models for different regulatory states of the locus. Work in other loci suggests a key role for CTCF and cohesin (subunit Rad21) in chromatin organisation and long distance regulatory interactions. ChIP-chip for CTCF/Rad21 across the Pax6 locus identified numerous sites within the gene and at distal regulatory locations. The majority of these sites are cell type invariable. The active enhancer modification H3K27ac identified both known and several novel putative enhancer elements distributed through the locus that are highly cell type specific. A subset of CTCF/Rad21 sites also acquire the active enhancer modification H3K27ac in a cell type dependent manor, suggesting that CTCF/Rad21 may facilitate looping to the target gene from these sites. Using reporter based assays, putative regulatory elements marked by the looping factors and active histone modifications showed a diverse range of functional activities. Unexpectedly only 3 of the 7 CTCF sites tested showed classical insulator activity in an enhancer blocking reporter assay. Surprisingly the strongest insulator tested resided within intron 7 the Pax6 gene. Other CTCF/Rad21 sites were neutral or enhancers in the insulator assay. This reveals the disparity between predicting regulatory properties using ChIP binding profiles alone and the actual outcome of functional reporter experiments. A novel element, CTCF6 showed a ChIP signature of CTCF/Rad21/H3K27ac in all Pax6 expressing tissues, and functioned as a strong enhancer in transient transfection and stable LacZ reporter assays. CTCF6 recapitulated a broad range of Pax6 expression patterns, at multiple embryonic stages, including the brain, neural tube and pancreas. A second novel element, E-120 identified in the pancreatic derived cell line, drove stable embryonic reporter expression in the embryonic pancreas and sub set of brain regions. Together this has expanded the repertoire and size of Pax6’s regulatory landscape particular in the upstream region. Chromatin conformation capture (3C) was used to characterise the…

Subjects/Keywords: 572.8; Pax6; gene regulation; chromatin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Buckle, A. J. (2014). Regulatory architecture of the Pax6 locus. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/16878

Chicago Manual of Style (16^th Edition):

Buckle, Adam James. “Regulatory architecture of the Pax6 locus.” 2014. Doctoral Dissertation, University of Edinburgh. Accessed July 16, 2019. http://hdl.handle.net/1842/16878.

MLA Handbook (7^th Edition):

Buckle, Adam James. “Regulatory architecture of the Pax6 locus.” 2014. Web. 16 Jul 2019.

Vancouver:

Buckle AJ. Regulatory architecture of the Pax6 locus. [Internet] [Doctoral dissertation]. University of Edinburgh; 2014. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1842/16878.

Council of Science Editors:

Buckle AJ. Regulatory architecture of the Pax6 locus. [Doctoral Dissertation]. University of Edinburgh; 2014. Available from: http://hdl.handle.net/1842/16878

Rutgers University

22. Caratozzolo, Rose Marie, 1978-. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.

Degree: PhD, Biochemistry, 2011, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

►

The 3’-end processing of nearly all eukaryotic pre-mRNAs comprises multiple steps which culminate in the addition of a poly(A) tail, which is essential for mRNA… (more)

▼

The 3’-end processing of nearly all eukaryotic pre-mRNAs comprises multiple steps which culminate in the addition of a poly(A) tail, which is essential for mRNA stability, translation, and export. Consequently, polyadenylation regulation is an important component of gene expression. One way to regulate polyadenylation is to inhibit the activity of a single poly(A) site, as exemplified by the U1A protein that negatively autoregulates itself by binding to a Polyadenylation Inhibitory Element (PIE) site within the 3’ UTR of its own pre-mRNA. U1 snRNP, which is primarily involved in splice site recognition, inhibits poly(A) site activity in papillomaviruses by binding to 5’ splice site-like sequences, which have recently been named “U1-sites”. Here, a recently identified U1-site in the human U1A 3'UTR is examined and shown to synergize with the adjacent PIE site to inhibit polyadenylation. However, unlike the sites found in papillomaviruses, the U1A U1-site has no inhibitory activity on its own and is dependent on a wild-type PIE. This lack of activity is due to the site being masked within a phylogenetically conserved stem structure (U1-STEM). The secondary RNA structure of this region was confirmed by RNase digestion analysis. Mutation of the U1-STEM, thereby opening up the U1-site, greatly increases U1-site mediated inhibition. The region between the U1-STEM and PIE (referred to as Region C) was also revealed to be required for synergy. Since biotin pulldown assays indicated that U1 snRNP binding to the U1-site was not affected by the presence of the U1-STEM, a model was proposed suggesting that U1 snRNP binds to the U1-STEM, but remains trapped in an inactive conformation until PIE is bound by two U1A molecules. However, further experiments showed that U1 snRNP binding did actually increase when the U1-STEM was mutated, but no corresponding change to the U1-STEM structure was detected. The discrepancies within these data suggest there is still much to be determined regarding the binding of U1 snRNP to the U1-Site. A more refined model is then presented which involves remodeling of Region C and part of the U1-STEM.

Advisors/Committee Members: Caratozzolo, Rose Marie, 1978- (author), GUNDERSON, SAMUEL I (chair), Brewer, Gary (internal member), Covey, Lori (internal member), Tian, Bin (outside member).

Subjects/Keywords: Gene expression; Genetic regulation; RNA

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Caratozzolo, Rose Marie, 1. (2011). Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. (Doctoral Dissertation). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

Chicago Manual of Style (16^th Edition):

Caratozzolo, Rose Marie, 1978-. “Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.” 2011. Doctoral Dissertation, Rutgers University. Accessed July 16, 2019. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530.

MLA Handbook (7^th Edition):

Caratozzolo, Rose Marie, 1978-. “Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.” 2011. Web. 16 Jul 2019.

Vancouver:

Caratozzolo, Rose Marie 1. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. [Internet] [Doctoral dissertation]. Rutgers University; 2011. [cited 2019 Jul 16]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530.

Council of Science Editors:

Caratozzolo, Rose Marie 1. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. [Doctoral Dissertation]. Rutgers University; 2011. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

University of Texas – Austin

23. -1259-2181. Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster.

Degree: Ecology, Evolution and Behavior, 2016, University of Texas – Austin

URL: http://hdl.handle.net/2152/46829

► Understanding variation in form and behavior within and among species requires mapping genotypes to phenotypes. Much of this variation depends on differences in regulatory DNA… (more)

▼ Understanding variation in form and behavior within and among species requires mapping genotypes to phenotypes. Much of this variation depends on differences in regulatory DNA scattered throughout the genome; in the context of behavior, these regulatory sequences govern gene expression in regions of the brain that shape behavior. Surprisingly few studies have characterized the regulatory changes that underlie the adaptive evolution of brain and behavior. In my PhD dissertation project, I investigated the adaptive role of gene regulation in the evolution of pair-bonding and sexual fidelity in the prairie voles, Microtus ochrogaster. Expression of Avpr1a in the ventral pallidum plays a critical role in the origin and evolution of pair-bonding in these monogamous voles. In Chapter 1, I have applied phylogenetic and population genetic methods to find signatures of selection in functional elements in the prairie vole genome. I identified a regulatory element of the Avpr1a locus that is under positive selection, this sequence coincides with the origins of expression of this gene in a reward region, the ventral pallidum. Then, I tested its causality using transgenic mouse enhancer assays. I found that transgenic mice expressing a reporter under the control of this prairie vole enhancer were able to drive expression in the ventral pallidum, but expression was sensitive to insertion site. Interestingly, this gene also shows profound differences between individuals. In Chapter 2, I applied population genomic tools to demonstrate that this locus shows signatures of balancing selection in a polymorphic enhancer that predicts expression in a spatial memory circuit. I found that alleles that predict aspects of space use and sexual fidelity are strongly linked to each other. Moreover, I show evidence that the evolution of this regulatory element seems to be mediated by a mix of balancing, epistatic and density-dependent selection. In Chapter 3, I performed RNA-sequencing experiments to analyze monogamy-related genomic changes in the brain. I found massive changes in gene expression of prairie voles in contrast to promiscuous meadow voles, despite their gene expression modules are very well preserved. Moreover, neuroplasticity –a neural process involved with learning— was strongly activated in prairie but not it meadow vole brains. Overall, the results of these experiments reveal the potential for gene regulation to drive the adaptive evolution of complex behaviors. Advisors/Committee Members: Phelps, Steven Michael, 1970- (advisor), Hofmann, Johan (committee member), Matz, Mikhail V (committee member), Atkinson, Nigel S (committee member), Juenger, Thomas E (committee member).

Subjects/Keywords: Behavior; Evolution; Gene; Regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

-1259-2181. (2016). Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster. (Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46829

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

-1259-2181. “Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster.” 2016. Thesis, University of Texas – Austin. Accessed July 16, 2019. http://hdl.handle.net/2152/46829.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

-1259-2181. “Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster.” 2016. Web. 16 Jul 2019.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-1259-2181. Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster. [Internet] [Thesis]. University of Texas – Austin; 2016. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/2152/46829.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

-1259-2181. Gene regulatory evolution and the origin of complex behaviors in the prairie vole, Microtus ochrogaster. [Thesis]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/46829

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center

24. Young, Melissa Rasar. Paxillin is a Novel Regulator of Xenopus Oocyte Maturation.

Degree: 2010, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/786

► Oocyte maturation is triggered by steroids in a transcription-independent fashion that involves an unusual positive feedback loop whereby MOS (a germ cell specific Raf) activates… (more)

Subjects/Keywords: Oocytes; Paxillin; Gene Expression Regulation

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APA (6^th Edition):

Young, M. R. (2010). Paxillin is a Novel Regulator of Xenopus Oocyte Maturation. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/786

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Young, Melissa Rasar. “Paxillin is a Novel Regulator of Xenopus Oocyte Maturation.” 2010. Thesis, University of Texas Southwestern Medical Center. Accessed July 16, 2019. http://hdl.handle.net/2152.5/786.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Young, Melissa Rasar. “Paxillin is a Novel Regulator of Xenopus Oocyte Maturation.” 2010. Web. 16 Jul 2019.

Vancouver:

Young MR. Paxillin is a Novel Regulator of Xenopus Oocyte Maturation. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2010. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/2152.5/786.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Young MR. Paxillin is a Novel Regulator of Xenopus Oocyte Maturation. [Thesis]. University of Texas Southwestern Medical Center; 2010. Available from: http://hdl.handle.net/2152.5/786

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

25. Lang, Kevin. Transcriptional regulation of incompatibility type A/C plasmids.

Degree: PhD, Comparative and Molecular Biosciences, 2015, University of Minnesota

URL: http://hdl.handle.net/11299/174866

► Plasmids are extrachromosomal DNA elements that often carry beneficial phenotypes for the bacterial host. Incompatibility type A/C (IncA/C) plasmids are large (~100 ~ 200 kilobases… (more)

▼ Plasmids are extrachromosomal DNA elements that often carry beneficial phenotypes for the bacterial host. Incompatibility type A/C (IncA/C) plasmids are large (~100 ~ 200 kilobases (kb)), conjugative plasmids that are carried by Gram-negative bacteria. IncA/C plasmids often carry numerous genes that confer resistance to antimicrobials and have been isolated from many types of bacteria that pose significant risks in both human and animal medicine. Although IncA/C plasmids have been described in the literature for many years, little is known about their basic biology. For the past decade, many fully sequenced IncA/C variants have been described. There has been a lack of work concerning core functions of these plasmids, such as, replication, conjugative transfer and maintenance. This dissertation focuses on how these plasmids are regulated on a transcriptional level. We used pAR060302, a prototypical IncA/C plasmid, to conduct several experiments investigating exactly what genes are transcribed and how different conditions affect their transcriptional landscape. RNA-Seq was used to understand how antimicrobial exposure can affect the way genes are expressed on IncA/C plasmids. We found that, under the conditions we tested, antimicrobials have little effect on the transcription of genes on pAR060302. However, this initial study was the first to explore genes carried IncA/C plasmids in terms of their expression. Further RNA-Seq experiments were carried out in several different bacterial genera all carrying the same IncA/C plasmid, pAR060302. These experiments attempted to characterize how a broad host-range plasmid, such as IncA/C, might be differentially regulated in different hosts. We found that only subtle changes occur in the expression of plasmid genes. Carriage of IncA/C plasmids was found to have diverse effects on chromosomal gene expression. Genes involved in 2-carbon metabolism in Escherichia coli are up-regulated due to plasmid carriage. Our results suggest that plasmid encoded factors might serve varying levels of importance depending on the host chromosomal background. Experiments were carried out on E. coli carrying plasmids with mutations in a group of predicted transcriptional regulators to determine their function. We identified the positive regulators of conjugative transfer in IncA/C plasmids, acaD and acaC. We also found a repressor of transfer, acr2, which encodes an H-NS-like protein. We further show that acr2 might regulate genes beyond those that are involved in conjugative transfer. This dissertation builds on our understanding on what mechanisms are important for the maintenance of large plasmids in Gram-negative bacteria. Understanding how plasmids might specifically tune host metabolism to improve competitive fitness would impact what evolutionary processes were involved in their emergence. Characterization of regulatory networks that govern core plasmid processes, such as conjugation, might assist in the development of new models of how these plasmids disseminate throughout bacterial…

Subjects/Keywords: antibiotic resistance; gene regulation; Plasmids

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lang, K. (2015). Transcriptional regulation of incompatibility type A/C plasmids. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/174866

Chicago Manual of Style (16^th Edition):

Lang, Kevin. “Transcriptional regulation of incompatibility type A/C plasmids.” 2015. Doctoral Dissertation, University of Minnesota. Accessed July 16, 2019. http://hdl.handle.net/11299/174866.

MLA Handbook (7^th Edition):

Lang, Kevin. “Transcriptional regulation of incompatibility type A/C plasmids.” 2015. Web. 16 Jul 2019.

Vancouver:

Lang K. Transcriptional regulation of incompatibility type A/C plasmids. [Internet] [Doctoral dissertation]. University of Minnesota; 2015. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/11299/174866.

Council of Science Editors:

Lang K. Transcriptional regulation of incompatibility type A/C plasmids. [Doctoral Dissertation]. University of Minnesota; 2015. Available from: http://hdl.handle.net/11299/174866

University of New Mexico

26. Morriss, Ginny. Identification of the wings apart transcriptional unit in Drosophila melanogaster.

Degree: UNM Biology Department, 2012, University of New Mexico

URL: https://digitalrepository.unm.edu/biol_etds/84

► Muscle development is an evolutionarily conserved process. Mechanisms that govern the development of specific muscles in invertebrates can inform our understanding of how vertebrate muscles… (more)

Subjects/Keywords: myogenesis; development; gene regulation; Drosophila

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APA (6^th Edition):

Morriss, G. (2012). Identification of the wings apart transcriptional unit in Drosophila melanogaster. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biol_etds/84

Chicago Manual of Style (16^th Edition):

Morriss, Ginny. “Identification of the wings apart transcriptional unit in Drosophila melanogaster.” 2012. Doctoral Dissertation, University of New Mexico. Accessed July 16, 2019. https://digitalrepository.unm.edu/biol_etds/84.

MLA Handbook (7^th Edition):

Morriss, Ginny. “Identification of the wings apart transcriptional unit in Drosophila melanogaster.” 2012. Web. 16 Jul 2019.

Vancouver:

Morriss G. Identification of the wings apart transcriptional unit in Drosophila melanogaster. [Internet] [Doctoral dissertation]. University of New Mexico; 2012. [cited 2019 Jul 16]. Available from: https://digitalrepository.unm.edu/biol_etds/84.

Council of Science Editors:

Morriss G. Identification of the wings apart transcriptional unit in Drosophila melanogaster. [Doctoral Dissertation]. University of New Mexico; 2012. Available from: https://digitalrepository.unm.edu/biol_etds/84

Rice University

27. Ruths, Troy. Population Regulomics: Applying population genetics to the cis-regulome.

Degree: PhD, Engineering, 2014, Rice University

URL: http://hdl.handle.net/1911/77508

► Population genetics provides a mathematical and computational framework for understanding and modeling evolutionary processes, and so it is vital for the investigation of biological systems.… (more)

▼ Population genetics provides a mathematical and computational framework for understanding and modeling evolutionary processes, and so it is vital for the investigation of biological systems. In its current state, molecular population genetics is exclusively focused on molecular sequences (DNA, RNA, or amino acid sequences), where all application-ready simulators and analytic measures work only on sequence data. Consequently, in the early 2000s, when technologies became available to sequence entire genomes, population genetic approaches were naturally applied to mine out signatures of selection and conservation, resulting in the subfi eld of population genomics. Nearly every present genome project applies population genomic techniques to identify functional information and genome structure. Recent technologies have ushered in a similar wave of genetic information, this time focusing on biological mechanisms operating above the genome, most notably on gene regulation (regulatory networks). In this work, I develop a molecular population genetics approach for gene regulation, called population regulomics, which includes simulators and analytic measurements that operate on populations of regulatory networks. I conducted extensive data analyses to connect the genome with the cis-regulome, developed computationally effi cient simulators, and adapted population genetic measurements on sequence to the regulatory network. By connecting genomic information to cis-regulation, we may apply the wealth of knowledge at the genome level to observed patterns at the regulatory level with unknown evolutionary origin. I demonstrate that by applying population regulomics to the E. coli cis-regulatory network, for the rst time we are able to quantify the evolutionary origins of topological patterns and reveal the surprising amount of neutral signal in the bacterial cis-regulome. Since regulatory networks play a central role in cellular functioning and, consequently, organismal fitness, this new sub-fi eld of population regulomics promises to shed the light of evolution on regulatory mechanisms and, more broadly, on the genetic mechanisms underlying the various phenotypes. Advisors/Committee Members: Nakhleh, Luay K. (advisor), Jermaine, Christopher M. (committee member), Kavraki, Lydia E. (committee member), Kohn, Michael H. (committee member).

Subjects/Keywords: Population genetics; Simulation; Gene regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ruths, T. (2014). Population Regulomics: Applying population genetics to the cis-regulome. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/77508

Chicago Manual of Style (16^th Edition):

Ruths, Troy. “Population Regulomics: Applying population genetics to the cis-regulome.” 2014. Doctoral Dissertation, Rice University. Accessed July 16, 2019. http://hdl.handle.net/1911/77508.

MLA Handbook (7^th Edition):

Ruths, Troy. “Population Regulomics: Applying population genetics to the cis-regulome.” 2014. Web. 16 Jul 2019.

Vancouver:

Ruths T. Population Regulomics: Applying population genetics to the cis-regulome. [Internet] [Doctoral dissertation]. Rice University; 2014. [cited 2019 Jul 16]. Available from: http://hdl.handle.net/1911/77508.

Council of Science Editors:

Ruths T. Population Regulomics: Applying population genetics to the cis-regulome. [Doctoral Dissertation]. Rice University; 2014. Available from: http://hdl.handle.net/1911/77508

University of California – San Francisco

28. Dalton, Ryan P. Chemoreceptor Feedback by the Unfolded Protein Response.

Degree: Neuroscience, 2015, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/0z78b1sw

► Each olfactory sensory neuron (OSN) expresses exactly one olfactory receptor (OR) gene, a feature which requires both a limiting or inefficient process of OR transcriptional… (more)

Subjects/Keywords: Cellular biology; gene regulation; olfaction

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APA (6^th Edition):

Dalton, R. P. (2015). Chemoreceptor Feedback by the Unfolded Protein Response. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/0z78b1sw

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dalton, Ryan P. “Chemoreceptor Feedback by the Unfolded Protein Response.” 2015. Thesis, University of California – San Francisco. Accessed July 16, 2019. http://www.escholarship.org/uc/item/0z78b1sw.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dalton, Ryan P. “Chemoreceptor Feedback by the Unfolded Protein Response.” 2015. Web. 16 Jul 2019.

Vancouver:

Dalton RP. Chemoreceptor Feedback by the Unfolded Protein Response. [Internet] [Thesis]. University of California – San Francisco; 2015. [cited 2019 Jul 16]. Available from: http://www.escholarship.org/uc/item/0z78b1sw.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dalton RP. Chemoreceptor Feedback by the Unfolded Protein Response. [Thesis]. University of California – San Francisco; 2015. Available from: http://www.escholarship.org/uc/item/0z78b1sw

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cincinnati

29. GHANEM, AMER. A Modular Gene Regulation Network Model of Artificial Ontogenesis.

Degree: MS, Engineering : Computer Science, 2008, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204580560

► A fundamental issue in evolution is the balance between variation and stability. Change isnecessary for the evolution of fitter forms, but it cannot come at… (more)

▼ A fundamental issue in evolution is the balance between variation and stability. Change isnecessary for the evolution of fitter forms, but it cannot come at the expense of disruptingstructures or processes that are critical to survival. The mechanisms that allow sufficientvariation to occur while preserving critical features are, therefore, central to evolvability -the viability of the evolutionary process in a class of systems. Recent work in evolutionarydevelopmental biology has demonstrated that modularity is the key enabler for balancingvariation and stability in animals. The deployment of the same developmental modules indifferent spatial and temporal combinations (called heterotopy and heterochrony, respec-tively) can generate a wide range of forms without the need for much change within themodules. Thus, useful and sometimes critical features evolved with great difficulty can beconserved as modules, while large changes in the regulatory mechanisms underlying their usecan provide the variation needed for evolution. In this thesis, we combine the idea of regula-tory variation in a modular developmental system with Kauffmans hypothesis of cell typesas attractors. We present a simple model for the ontogenesis of two-dimensional shapes anattractor network of regulatory genes controls the deployment of genetic network modulesthat explicitly determine growth and phenomenological attributes. We use this model toshow that:1. A very wide variety of forms can be generated purely through changes in the connec-tivity and input weights of the regulatory network while conserving the rest of thenetwork.2. Systematic variations in the switching conditions for a fixed set of regulatory attractorsproduce systematic changes in the phenotypes, effectively generating a phylogeny.3. Small variations in the initial conditions (distribution of maternal proteins, etc.) pro-duces minimal phenotypic changes, somewhat larger variations generate phenotypeswith a family resemblance, and much larger ones produce distinct phenotypes.In the future, we plan to extend the model to three-dimensional shapes and incorporateit into an evolutionary algorithm for generating more complex functional phenotypes. Advisors/Committee Members: Minai, Ali (Committee Chair).

Subjects/Keywords: Computer Science; Artificial ontogenesis; Modular Gene regulation; Gene regulation network

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

GHANEM, A. (2008). A Modular Gene Regulation Network Model of Artificial Ontogenesis. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204580560

Chicago Manual of Style (16^th Edition):

GHANEM, AMER. “A Modular Gene Regulation Network Model of Artificial Ontogenesis.” 2008. Masters Thesis, University of Cincinnati. Accessed July 16, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204580560.

MLA Handbook (7^th Edition):

GHANEM, AMER. “A Modular Gene Regulation Network Model of Artificial Ontogenesis.” 2008. Web. 16 Jul 2019.

Vancouver:

GHANEM A. A Modular Gene Regulation Network Model of Artificial Ontogenesis. [Internet] [Masters thesis]. University of Cincinnati; 2008. [cited 2019 Jul 16]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204580560.

Council of Science Editors:

GHANEM A. A Modular Gene Regulation Network Model of Artificial Ontogenesis. [Masters Thesis]. University of Cincinnati; 2008. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204580560

Vanderbilt University

30. Lind, Abigail Lee. The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus.

Degree: MS, Biomedical Informatics, 2014, Vanderbilt University

URL: http://etd.library.vanderbilt.edu//available/etd-11142014-143959/ ;

► Filamentous fungi produce diverse secondary metabolites (SMs) essential to their ecology and adaptation. Although each SM is typically produced by only a handful of species,… (more)

Subjects/Keywords: gene regulation; evolution; evolution; aspergillus; aspergillus; gene regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lind, A. L. (2014). The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus. (Masters Thesis). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-11142014-143959/ ;

Chicago Manual of Style (16^th Edition):

Lind, Abigail Lee. “The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus.” 2014. Masters Thesis, Vanderbilt University. Accessed July 16, 2019. http://etd.library.vanderbilt.edu//available/etd-11142014-143959/ ;.

MLA Handbook (7^th Edition):

Lind, Abigail Lee. “The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus.” 2014. Web. 16 Jul 2019.

Vancouver:

Lind AL. The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus. [Internet] [Masters thesis]. Vanderbilt University; 2014. [cited 2019 Jul 16]. Available from: http://etd.library.vanderbilt.edu//available/etd-11142014-143959/ ;.

Council of Science Editors:

Lind AL. The Evolution of Secondary Metabolism and Development Regulation in the Fungal Genus Aspergillus. [Masters Thesis]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu//available/etd-11142014-143959/ ;

Open Access Theses and Dissertations