Dissertations / Theses on the topic 'Bacteriophages – Molecular genetics; Genetic transcription'

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1

Dibbens, Justin Andrew. "Studies on the control of late gene transcription in coliphage 186 /." Title page, contents and summary only, 1990. http://web4.library.adelaide.edu.au/theses/09PH/09phd543.pdf.

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2

Kalionis, Bill. "The early control region of temperate coliphage 186 : sequence and transcription studies /." Title page, contents and summary only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phk14.pdf.

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3

Folberg, Adriana. "Murine Hoxd4 : characterization of the transcription unit and genetic interactions with retinoic acid receptors." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35881.

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Hox genes encode homeodomain-containing transcription factors involved in the specification of structures along the anterior-posterior and secondary axes of the vertebrate embryo. Many pieces of evidence suggest that retinoic acid (RA) regulates Hox gene function. The present work involved the characterization of the transcription unit of a murine Hox gene, Hoxd4, its response to RA and its genetic interactions with Retinoic Acid Receptors (RARs) beta and gamma.
We have identified two Hoxd4 transcription start sites, P1 and P2. Multiple transcripts were identified by Northern blot, originating from both promoters and multiple polyadenylations signals. Expression of P1 transcripts in the neural tube showed an anterior border at the rhombomere 6/7 boundary, while P2 transcripts are detected more posteriorly. Somitic expression was strong up to somite 6 and weak in somite 5. After RA exposure in utero, only P1 showed a direct response to exogenous RA in the hindbrain, 4 or 24 hours after RA treatment on day 8.5 of gestation. In embryos collected 24 hours after RA treatment, wild-type mice showed a full rhombomere anteziorization of Hoxd4 expression. In contrast, Rarb null mice displayed only a partial anteriorization under the same conditions. The same holds true for the Hoxb4 gene. These results indicate that RARbeta is one of the mediators of the Hoxd4 and Hoxb4 RA-response.
Rarg null mutant mice display homeotic transformations of the cervical vertebrae that are similar to a Hoxd4 null mutant phenotype. In order to examine whether Hoxd4 and Rarg he in a common genetic pathway for patterning of the cervical region, we generated mice doubly mutant for these genes and analyzed their skeletons. For two malformations present in single mutants, namely an ectopic anterior arch in cervical vertebra 2 (C2) and the fusion of the basioccipital bone to C1, the penetrance and expressivity in double null mutants was significantly increased. Thus, we conclude that Hoxd4 and Rarg interact synergistically in the specification of these cervical vertebrae. In contrast to Rarg mutants, retinoic acid treatment of Hoxd4; Rarg double mutants on day 10.5 does not rescue normal development of C2. This result suggests that Hoxd4 mediates the retinoic acid-induced correction of this phenotype in Rarg mutants.
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4

Kwong, Ka-yee, and 鄺嘉儀. "Pituitary-specific transcription factor PIT-1 in Chinese grass carp: molecular cloning, functionalcharacterization, and regulation of its transcript expression at thepituitary level." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29474991.

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5

Lee, Sungkeun. "Molecular genetic analysis of nucleotide excision repair genes in Dictyostelium discoideum /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841209.

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6

Jiang, Yonghua. "Molecular cloning of AP-1 transcription factors in Chinese grass carp and their functional roles in PACAP-stimulated growth hormone geneexpression." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245419.

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7

Mavris, Maria. "Bacteriophage SfII mediated serotype conversion in Shigella flexneri /." Title page, abstract and contents only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm4608.pdf.

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8

Al, Zamal Faiyaz. "Relating the expression-based and sequence-based estimates of regulation in the gap gene system of Drosophila melanogaster." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112321.

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Quantitative analysis of Drosophila melanogaster gap gene expression data reveals valuable information about the nature and strengths of interactions in the gap gene network. We first explore different models for fitting the spatiotemporal gene expression data of Drosophila gap gene system and validate our results by computational analysis and comparison with the existing literature. A fundamental problem in systems biology is to associate these results with the inherent cause of gene regulation, namely the binding of the transcription factors (TF) to their respective binding sites. In order to relate these expression-based estimates of gap gene regulation with the sequence-based information of TF binding site composition, we also explore two related problems of (i) finding a set of regulatory weights that is proportional to the binding site occupancy matrix of the transcription factors in current literature and (ii) finding a set of position weight matrices of the TFs that produce a new binding site occupancy matrix showing a greater level of proportionality with our regulatory weights. Our solution to the first problem yielded a regulatory weight matrix incapable of explaining the true causes of gene expression profile despite its relative numerical accuracy in predicting the gene expressions. On the other hand, the second optimization problem could be solved up to a reasonable level of accuracy, but further analysis on the result demonstrated that this optimization problem may be under-constrained. We devise a simple regularization strategy that helps us to reduce the under-constrained nature of the problem.
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9

Fung, Sai-kit, and 馮世傑. "Grass carp activin: molecular cloning and functional role in regulating growth hormone gene expression in grasscarp pituitary cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30455947.

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10

Lam, Ka-man Amy, and 林嘉敏. "Osmotic response element binding protein (OREBP) is an essential regulator of urine concentrating mechanism and renal protection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B3127402X.

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11

Fu, Guodong, and 傅國棟. "Grass carp CREB: molecular cloning, regulation of gene expression and functional implications at thepituitary level." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B3843751X.

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12

Engström, Pär. "Gene complexes and regulatory domains in metazoan genomes /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-361-0/.

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13

Yu, Sung-Lim. "Analysis of the response of nucleotide excision repair genes in Dictyostelium discoideum /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841196.

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14

Vasanthavada, Keshav. "Generation of cDNA chips from the black widow spider, latrodectus hesperus, for gene discovery and expression profiling using microarray technology, and molecular characterization of a novel silk glue protein." Scholarly Commons, 2005. https://scholarlycommons.pacific.edu/uop_etds/624.

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eDNA microarray technology has generated a tremendous amount of interest among biologists because of its promise to monitor the entire genome on a single chip, thus enabling researchers to have a better picture of the interaction among thousands of genes simultaneously. In the current study, this technology was used to print over 3,000 unknown genes from various silk glands of the black widow spider to profile their expression patterns and to identify novel candidates. Spiders are remarkable creatures because of their ability to make different silks, each with a specific function. Some of these silks have amazing mechanical properties, comparable to those of the finest synthetic materials. Several silk genes have been cloned from various spiders over the last few years, and the contribution of each of those genes in silk production has been identified. However, the majority of cellular and biochemical processes involved in silk manufacture remain a mystery. In our research, we attempt to identify genes that might be involved in silk assembly, on a global scale and investigate more about those genes and their interplay with other key biological molecules involved in silk manufacture. Our study showed that silking spiders for a certain period of time resulted in down-regulation of two important silk genes, ECP-1 and ECP-2. Both these genes are key molecules implicated for their role in maintaining the egg case architecture in the black widow spider.,-and we believe that these genes are also directly or indirectly involved in the manufacture of dragline silk. Microarray analyses also enable the discovery of several other interesting molecules, two of which could be accessory proteins involved in silk formation. Furthermore, in a separate study we also characterized a novel silk glue protein with unique ensemble repeats. In conclusion, we believe that the findings of this study will indeed be significant to silk researchers and material scientists alike and it will enhance our knowledge in understanding the mystery behind silk production.
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15

Andersen, Malin. "Computational and experimental approaches to regulatory genetic variation." Doctoral thesis, Stockholm : Bioteknologi, Kungliga Tekniska högskolan, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-4593.

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16

O'Leary, Debra Alison. "Characterisation of gene structure and function of the ETS transcription factor Gabpα in mouse." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9445.

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17

Xu, Minzhen. "Regulation of Transcription of Mouse Immunoglobulin Germ-Line γ1 RNA: Structural Characterization of Germ-Line γ1 RNA and Molecular Analysis of the Promoter: A Dissertation." eScholarship@UMMS, 1991. https://escholarship.umassmed.edu/gsbs_diss/99.

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The antibody class switch is achieved by DNA recombination between the sequences called switch (S) regions located 5' to immunoglobulin (Ig) heavy chain constant (CH) region genes. This process can be induced in cultured B cells by polyclonal stimulation and switching can be directed to specific antibody classes by certain lymphokines. These stimuli may regulate the accessibility of CH genes and their S regions to a recombinase as indicated by hypomethylation and transcriptional activity. For example, RNAs transcribed from specific unrearranged (germ-line) CH genes are induced prior to switching under conditions that promote subsequent switching to these same CH genes. The function of transcription of these germ-line CH genes is unknown. How stimuli regulate the accessibility of CHgenes is also unclear. I report in this dissertation the structure of the RNA transcribed from the unrearranged Cγ1 gene in mouse spleen cells treated with LPS plus a HeLa cell supernatant containing recombinant interleukin 4 (rIL-4). I will also show that an 150-bp region upstream of the first initiation site of germ-line γ1 RNA contains promoter and enhancer elements responsible for basal level expression and inducibility by phorbol 12-myristate 13-acetate (PMA) and synergy with IL-4 in an IgM+ B cell line, L10A6.2, and an IgG2a+B cell line, A20.3. The germ-line γ1 RNA is initiated at multiple start sites 5' to the tandem repeats of the γ1 switch (Sγ1) region. As is true for analogous RNAs transcribed from other unrearranged genes, the germ-line γ1 RNA has an I exon transcribed from the region 5' to the Sγ1 region.. The Iγ1 exon is spliced at a unique site to the Cγ1 gene. The germ-line γ1 RNA has an open-reading frame (ORF) that potentially encodes a small protein 48 amino acids in length. Elements located within the 150 bp region 5' to the first initiation site of germ-line γ1 RNA are necessary and sufficient to confer inducibility by PMA and synergy with IL-4 to a minimal thymidine kinase (TK) promoter in L10A6.2 cells but are not sufficient to confer this inducibility in A20.3 cells. Linker-scanning mutations demonstrated that these multiple elements function in a mutually dependent manner as indicated by the fact that mutation of any single element will decrease constitutive expression and inducibility by PMA and PMA plus IL-4. This 150-bp region contains several consensus sequences that bind to known or putative transcription factors, including a C/EBP binding site/IL-4 response element (in the promoter for Ia Aαkgene), four CACCC boxes, a PU box, a TGFβ inhibitory element (TIE), an interferon-αβ response element (αβIRE), and an AP-3 site. My results begin to provide a description of the mechanism of regulation of the accessibility of unrearranged germ-line Sγ1-Cγ1 gene. By activating the germ-line γ1 promoter, IL-4 induces transcription of germ-line γ1 RNA, thereby inducing accessibility of the Sγ1-Cγ1 gene. By inhibiting expression of the germ-line γ1 promoter, IFNγ and TGFβ down-regulate transcription of germ-line γ1 RNA, thus reducing the accessibility of the Sγ1-Cγ1 gene. My results also suggest that signaling via the antigen receptor on B cells may be involved in induction of switch to IgG1. Furthermore, this is the first case reported in which multiple functionally interdependent elements are needed to respond to PMA.
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18

Hartt, Gregory Thomas. "Regulation of the human neuronal nitric oxide synthase gene via alternate promoters." Columbus, OH : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1056034844.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xii, 152 p. : ill., (some col.). Includes abstract and vita. Advisor: Anthony Young, Molecular, Cellular, and Developmental Biology Program. Includes bibliographical references (p. 137-150).
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19

Simms, Amy Nicole. "Examination of Neisseria gonorrhoeae opacity protein expression during experimental murine genital tract infection /." Download the dissertation in PDF, 2005. http://www.lrc.usuhs.mil/dissertations/pdf/Simms2005.pdf.

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20

Neufing, Petra. "Establishment of lysogeny in coliphage 186 / by Petra Neufing." Thesis, 1997. http://hdl.handle.net/2440/114493.

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21

Richardson, Helena E. "Defining the early lythic region of coliphage 186 and the control of middle gene transcription / by Helena Elizabeth Richardson." 1987. http://hdl.handle.net/2440/21419.

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Includes bibliography
219 leaves, [22] leaves of plates : ill ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1987
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22

Robins, William Paul. "Antitermination is operative in bacteriophage T7 and is largely dependent on one promoter." 2008. http://hdl.handle.net/2152/18110.

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The translocation of the T7 genome into the cell is a multistep process. Following adsorption, approximately 850bp of the 40kb linear genome is internalized to expose host-specific promoters in the leading end to transcription components. There are three strong early promoters, PA1, PA2, and PA3 on this leading 850 bp. Further T7 genome internalization is coupled to transcription and I have measured internalization rates to characterize the rate of transcription by E. coli RNA polymerase in vivo. E.coli RNAP internalizes the entire 40kb and distal parts of the genome are internalized nearly as efficiently and at the same rate as the leading end. I have shown that processivity is dependent on the antitermination element boxA, located 63 bp downstream from PA3, and on only one of the three early promoters. However, when any one of boxA, PA3, or the host antitermination factor nusB is mutated the efficiency, rate, and apparent processivity of transcription -- and thus the efficiency of genome internalization are all significantly reduced. The PA3 promoter, boxA, and E. coli nusB are all non-essential for T7 growth, but they confer a fitness benefit to wild-type phage by increasing the rate of genome internalization. In T7, the minimal requirement for antitermination is promoter PA3 and the boxA sequence. I have found that transcripts initiating at PA1 and PA2 are not effectively antiterminated by boxA, however those from PA3 alone do. Upon further investigation it was shown that there is a requirement for sequences upstream of the -35 hexamer of PA3 to confer full antitermination. After T7 expresses its own single-subunit RNA polymerase, bacteriophage T7 must shutoff host transcription via the phage proteins gp0.7 and gp2. In the absence of host RNAP shutoff, T7 DNA is degraded and the infection fails. I have found that the absence of either promoter PA3 or boxA,gene 2 is unnecessary for growth. These results argue the target for shutoff is actually antiterminating transcription.
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23

Richardson, Helena Elizabeth. "Defining the early lythic region of coliphage 186 and the control of middle gene transcription / by Helena Elizabeth Richardson." Thesis, 1987. http://hdl.handle.net/2440/21419.

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24

Dibbens, Justin Andrew. "Studies on the control of late gene transcription in coliphage 186 / by Justin Andrew Dibbens." Thesis, 1990. http://hdl.handle.net/2440/19275.

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25

Kaufman, Charles K. "Transcriptional regulation of epidermal differentiation." 2003. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3097127.

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26

Gonzalez, Antonio 1973. "Molecular genetic analysis of TTG1-dependent cell fate pathways identifies a combinatorial Myb/bHLH transcription factor network in Arabidopsis." 2008. http://hdl.handle.net/2152/18349.

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The discovery of the Arabidopsis ttg1 mutant almost three decades ago provided a unique opportunity for the study of how several cell fates and organ identity pathways are co-regulated. Besides showing a lack of flavonoid based pigments, the pleiotropic ttg1 mutant is also deficient for the development of several epidermal characters including plant hair cells (trichomes), the non-hair cells of the root and the mucilage-secreting cells of the seed coat epidermis. Ectopic expression of the maize R bHLH transcriptional regulator of the flavonoid pigment pathway could completely suppress all the ttg1 mutant phenotypes, providing the first clue to the nature of the control mechanisms governing TTG1-dependent traits. Because it was established that a bHLH and a Myb protein are required for the regulation of anthocyanin pigment production in several plant species and an Arabidopsis Myb gene was necessary for trichome initiation, the existence of bHLH and Myb proteins that would regulate all the TTG1-dependent developmental pathways was hypothesized. This study works towards the elucidation of the transcriptional control mechanisms that regulate the TTG1-dependent developmental pathways. The identification and characterization of a key regulator, EGL3, uncovered the redundant nature of bHLH proteins operating under the TTG1 regulatory umbrella. As a result, bHLH regulators were assigned to all TTG1-dependent epidermal cell fate pathways and new roles for previously identified bHLH proteins were revealed. Roles suggested in the literature for Arabidopsis Myb factors suspected of regulating the flavonoid pigment pathway were at odds with findings from other plant models. Analysis of Myb loss-of-function RNAi lines and TTG1:GR and GL3:GR fusion lines presented here provides a clarified understanding of the regulation of anthocyanin biosynthesis by the Myb/bHLH/WDrepeat complex in Arabidopsis. Missing from the combinatorial complex model is the Myb component controlling the differentiation of the seed coat epidermis. Work presented here characterizes Myb5 as the primary Myb regulator of this differentiation pathway and defines a new role for TT2 as partially redundant with Myb5 for testa epidermis development. Myb5 also plays a minor role in trichome development and PA biosynthesis. Thus pleiotropy among the TTG1-dependent Myb regulators previously unobserved is first noted here. A more complete Myb/bHLH combinatorial transcription factor network model for the regulation of the TTG1-dependent pathways is proposed based on the results of work presented in this dissertation.
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27

Warren, William Daniels. "Molecular and genetic studies on the structure and regulation of the cinnabar gene of Drosophila melanogaster." Phd thesis, 1990. http://hdl.handle.net/1885/140199.

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28

Zhou, Jiansheng. "The molecular mechanism of H2A. Bbd in chromatin transcriptional regulation." Phd thesis, 2006. http://hdl.handle.net/1885/148698.

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29

Mavris, Maria. "Bacteriophage SfII mediated serotype conversion in Shigella flexneri / by Maria Mavris." Thesis, 1998. http://hdl.handle.net/2440/19206.

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Includes bibliography (27 leaves).
109, [160] leaves : ill. ; 30 cm.
The isolation of bacteriophage SfII has provided information regarding the molecular mechanism by which modifications are carried out by the serotype converting bacteriophages of S. flexneri.
Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1998?
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30

Jairam, Sowmya. "Transcription regulation of the class II alcohol dehydrogenase 7 (ADH7)." Thesis, 2014. http://hdl.handle.net/1805/5412.

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Indiana University-Purdue University Indianapolis (IUPUI)
The class IV alcohol dehydrogenase (ADH7, µ-ADH, σ-ADH) efficiently metabolizes ethanol and retinol. ADH7 is expressed mainly in the upper gastrointestinal tract with no expression in the liver unlike the other ADHs, and is implicated in various diseases including alcoholism, cancer and fetal alcohol syndrome. Genome wide studies have identified significant associations between ADH7 variants and alcoholism and cancer, but the causative variants have not been identified. Due to its association with two important metabolic pathways and various diseases, this dissertation is focused on studying ADH7 regulation and the effects of variants on this regulation using cell systems that replicate endogenous ADH7 expression. We identified elements regulating ADH7 transcription and observed differences in the effects of variants on gene expression. A7P-G and A7P-A, two promoter haplotypes differing in a single nucleotide at rs2851028, had different transcriptional activities and interacted with variants further upstream. A sequence located 12.5 kb upstream (7P10) can function as an enhancer. These complex interactions indicate that the effects of variants in the ADH7 regulatory elements depend on both sequence and cellular context, and should be considered in interpretation of the association of variants with alcoholism and cancer. The mechanisms governing the tissue-specific expression of ADH7 remain unexplained however. We identified an intergenic region (iA1C), located between ADH7 and ADH1C, having enhancer blocking activity in liver-derived HepG2 cells. This enhancer blocking function was cell- and position- dependent with no activity seen in CP-A esophageal cells. iA1C had a similar effect on the ectopic SV40 enhancer. The CCCTC-binding factor (CTCF) bound iA1C in HepG2 cells but not in CP-A cells. Our results suggest that in liver-derived cells, iA1C blocks the effects of downstream ADH enhancers and thereby contributes to the cell specificity of ADH7 expression. Thus, while genetic factors determine level of ADH7 transcriptional activity, iA1C helps determine the cell specificity of transcription.
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31

Park, Soyoung. "In vivo analysis of human LHX3 enhancer regulation." Thesis, 2014. http://hdl.handle.net/1805/3807.

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Indiana University-Purdue University Indianapolis (IUPUI)
The LHX3 transcription factor is essential for pituitary gland and nervous system development in mammals. In humans, mutations in the LHX3 gene underlie combined pituitary hormone deficiency (CPHD) disease featuring deficits in anterior pituitary hormones and defects in the nervous system. The mechanisms that control temporal and spatial expression of the LHX3 gene are poorly understood. The proximal promoters of the human LHX3 gene are insufficient to guide expression in vivo and downstream elements including a conserved 7.9 kilobase (kb) enhancer region appear to play a role in tissue-specific expression in the pituitary and nervous system. In this study, I characterized the activity of this downstream enhancer region in regulating gene expression at the cellular level during development. Human LHX3 enhancer-driven Cre reporter transgenic mice were generated to facilitate studies of enhancer actions. The downstream LHX3 enhancer primarily guides gene transcription in αGSU-expressing cells secreting the TSHβ, LHβ or FSHβ hormones and expressing the GATA2 and SF1 transcription factors. In the developing nervous system, the enhancer serves as a targeting module for expression specifically in V2a interneurons. These results demonstrate that the downstream LHX3 enhancer is important in specific endocrine and neural cell types but also indicate that additional regulatory elements are likely involved in LHX3 gene expression in other cell types. Further, these studies demonstrate significant gonadotrope cell heterogeneity during pituitary development, providing insights into the cellular physiology of this key reproductive regulatory cell. The human LHX3 enhancer-driven Cre reporter transgenic mice provide a valuable tool for further developmental studies of cell determination and differentiation in the pituitary and nervous system. Furthermore understanding the regulation of human LHX3 gene will help develop tools to better diagnose and treat pituitary CPHD disease.
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