+publisher:"Texas A&M University" +contributor:("Golding, Michael C")

Texas A&M University

1. Pinzon Arteaga, Carlos Andres. PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS.

Degree: MS, Biomedical Sciences, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/187291

► There are more than 6,052 identified genetic mutations linked to disease in humans and animals. Thanks to the advent of gene editing based on programmable… (more)

▼ There are more than 6,052 identified genetic mutations linked to disease in humans and animals. Thanks to the advent of gene editing based on programmable nucleases and the advances in DNA sequencing and writing technologies, it is now possible to make precise changes in eukaryotic genomes with the potential to correct monogenic diseases, from affected cells, tissues, organisms and eventually whole populations. This is the concept behind therapeutic genome editing, which arises out of the idea that instead of pursuing palliative care, the ideal therapy for monogenic diseases would be to develop a method that can directly correct the disease-causing mutations. Many of these disease alleles have been have been unknowingly co-selected when performing phenotypic genetic selection on plants and animals. Although selected breeding has been successful in the establishment and improvement of many different strains of plants and breeds of animals, we have been propagating these disease alleles in the populations. One of these deleterious alleles is the Glycogen Branching Enzyme Deficiency (GBED), which is caused by a nonsense mutation (C > A) in the first exon of the GBE1 gene that severely disrupts glycogen metabolism. This mutation is lethal in homozygotes and an estimated 9% of Quarter Horse and Paint Horse lineages are heterozygote carriers. In this work, we corrected this mutation in a heterozygous cell line derived from a high genetic merit American Quarter Horse stallion, by using CRISPRCas9. The long-term goal is to use the corrected cell lines for somatic cell nuclear transfer (SCNT) thereby generating a cloned animal that maintains the genetic merit of its predecessor, but is free of the GBED mutation. Precise genome editing requires the introduction of a double stranded break (DSB) at an exact location in the genome and the correct DNA repair outcome. Although CRISPRCas9 has allowed for the introduction of precise DSBs in a very efficient manner, the lack of control over cell-autonomous repair mechanisms namely non-homologous end-joining (NHEJ) and homologous recombination (HR), is still the major bottle neck for seamless genome editing. The DNA-dependent protein kinase (DNA-PK), composed of the Ku 70 - Ku 80 heterodimer and the DNA-PK catalytic subunit (DNA-PKvcs), is best known as the NHEJ molecular sensor for DNA damage, but has been also identified as a pattern recognition receptor (PRR) that defends against the invasion of foreign nucleic acids. Here we devised a novel strategy that capitalizes on the natural ability of the Vaccinia virus (VACV) C16 protein that evolved as an elegant subversion mechanism to inhibit the detection of the VACV genome by the host cytoplasmic PRR defenses, specifically the Ku-mediated DNA sensing. Advisors/Committee Members: Long, Charles R (advisor), Golding, Michael C (advisor), Satterfield, Michael C (committee member).

Subjects/Keywords: genome editing; CRISPR; genetic engineering; CRISPR-Cas9

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APA (6^th Edition):

Pinzon Arteaga, C. A. (2017). PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/187291

Chicago Manual of Style (16^th Edition):

Pinzon Arteaga, Carlos Andres. “PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS.” 2017. Masters Thesis, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/187291.

MLA Handbook (7^th Edition):

Pinzon Arteaga, Carlos Andres. “PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS.” 2017. Web. 20 Jan 2021.

Vancouver:

Pinzon Arteaga CA. PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS. [Internet] [Masters thesis]. Texas A&M University; 2017. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/187291.

Council of Science Editors:

Pinzon Arteaga CA. PRECISE AND EFFICIENT THERAPEUTIC GENOME EDITING FOR THE CORRECTION OF GENETIC DISEASES IN ANIMALS. [Masters Thesis]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/187291

Texas A&M University

2. Burns, Gregory Willis. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.

Degree: MS, Biomedical Sciences, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151804

► After 40 years of research, in vitro systems for mammalian embryo production produce lower quality embryos than those derived from in vivo sources. Recent reports… (more)

▼ After 40 years of research, in vitro systems for mammalian embryo production produce lower quality embryos than those derived from in vivo sources. Recent reports have demonstrated that in vitro bovine oocyte maturation systems benefit from the addition of oocyte secreted factors, specifically Bone Morphogenic Protein 15 (BMP15) from heterologous sources. However, known amino acid sequence variation and species-specific patterns of post-translational glycosylation lead us to hypothesize that utilization of bovine-specific oocyte secreted factors would be more beneficial than the observed effects of heterologous factors. To test this hypothesis, wild type, bovine BMP15 was cloned using reverse transcriptase PCR from RNA obtained from bovine ovarian tissue. For improved detection and purification of the biologically active recombinant protein, a FLAG tag peptide sequence (Asp-Tyr-Lys-Asp-Asp-Asp-Asp-Lys) was incorporated into the wild type BMP15 gene by PCR. This modified protein was cloned into the pCDNA 3 mammalian expression vector. HEK-293 (human embryonic kidney 293) and FBK (fetal bovine kidney) cell lines were transfected via electroporation and then selected to homogeneity. Collection and purification of rbFL-BMP15 from conditioned medium was accomplished by incubation with anti-FLAG affinity gel and the use of 3X FLAG peptide for elution. Peptides of 15.4 kDa and 17 kDa were noted from the human HEK-293 transfected cell line, while in contrast, bovine FBK cells produced a single 17 kDa protein. Bioactivity and BMP receptor signaling specificity were ascertained using in vitro treatment of HeLa cells and Western blotting for the BMP signaling molecule phosphorylated-SMAD 1/5. Inhibition of this signaling cascade using dorsomorphin, a selective bone morphogenic protein receptor I inhibitor, demonstrated the purified proteins served as BMP15-like agonists. To examine the impact of our purified, bovine-specific peptides on oocyte maturation, cumulus oocyte complexes were in vitro matured for 24 hours in the presence of 100 ng/ml recombinant human BMP15 or rbFL-BMP15 from human or bovine cell lines. Real time quantitative PCR analysis of BMP15 stimulated genes, PTGS2 and TSG6, revealed statistically significant increases in transcript level for treatment with human BMP15 by a Dunnett’s test (p<0.05). In this report, however, we failed to detect a significant affect of rbFL-BMP15 on the gene expression of in vitro mature cumulus oocyte complexes at 24 hours with 100 ng/ml rbFL-BMP15. Future studies including differing time points and concentrations, along with the addition of GDF9 to form a possible heterodimer should be investigated for the possibility of improving bovine oocyte in vitro maturation. Advisors/Committee Members: Long, Charles R (advisor), Golding, Michael C (committee member), Li, Qinglei (committee member).

Subjects/Keywords: BMP15; IVM; TGFB; recombinant protein; FLAG; BMPRI; ART; cattle; bovine; COC; oocyte

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

APA (6^th Edition):

Burns, G. W. (2013). Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151804

Chicago Manual of Style (16^th Edition):

Burns, Gregory Willis. “Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.” 2013. Masters Thesis, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/151804.

MLA Handbook (7^th Edition):

Burns, Gregory Willis. “Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.” 2013. Web. 20 Jan 2021.

Vancouver:

Burns GW. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. [Internet] [Masters thesis]. Texas A&M University; 2013. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/151804.

Council of Science Editors:

Burns GW. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. [Masters Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151804

Texas A&M University

3. Veazey, Kylee Jordan. An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders.

Degree: PhD, Genetics, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/156462

► Observations from a number of independent laboratories indicate that ethanol has the capacity to act as a powerful epigenetic disruptor and potentially derail the process… (more)

▼ Observations from a number of independent laboratories indicate that ethanol has the capacity to act as a powerful epigenetic disruptor and potentially derail the process of cellular differentiation. The aim of this dissertation was to determine the epigenetic effects of alcohol on chromatin structure, the heritability of these effects in vitro and in vivo, and whether the severity of these alterations is tied to the differentiation state of the cell. First, we investigated the epigenetic impact of ethanol exposure in a murine neural stem cell model using chromatin immunoprecipitation, quantitative polymerase chain reaction (ChIP-qPCR) and RNA analysis. We found that two widely-studied histone modifications, trimethylated histone 3 lysine 4 (H3K4me3) and trimethylated histone 3 lysine 27 (H3K27me3), were disrupted at promoters of a panel of homeobox genes involved in neural development in the presence of alcohol, and that these disruptions do not correlate with changes in the expression of the examined genes. Second, we determined whether the disruption of chromatin structure caused by alcohol is heritable through cell division after an acute exposure in vitro. We monitored changes in H3K27me3, H3K4me3, and acetylation/demethylation of histone 3 lysine 9 (H3K9ac and H3K9me2, respectively) at the promoters of our candidate homeobox genes using ChIP-qPCR. We found that alterations in these marks persist beyond the window of exposure, and do not retain the same levels compared to controls after a recovery period in which ethanol is withdrawn. Furthermore, changes in the expression of these genes often occurred after recovery and again do not correlate with histone modifications present at their respective promoters. These alterations occur despite no indication of cell stress, but are associated with increased expression of genes involved in cell proliferation and neural lineage markers after recovery. A decrease in many oxidative stress pathway genes was also observed upon exposure that was rectified after recovery. Importantly, changes in the gene expression of histone methyltransferases and DNA methyltransferases were observed, with a concurrent change in DNA methylation. We next chose to determine if the observed alterations in chromatin structure also appear in vivo using a mouse model of early acute ethanol exposure. Pregnant dams injected with 2.9 g/kg ethanol at gestational day (GD) 7 were sacrificed at GD17, and the fetuses scored for ocular and forebrain defects. Levels of H3K27me3 were low at the promoters of many of the candidate genes in affected mice, and high levels of H3K9me2 specifically identified ethanol-affected mice, suggesting its potential as a marker for FASD phenotypes. Finally, we determined whether the epigenetic effects of ethanol are dependent on the differentiation state of the cell using a murine embryonic stem cell (ESC) model. Acute ethanol exposure resulted in oscillating changes in levels of histone modifications for a long as 10 days post-exposure. Despite these changes in… Advisors/Committee Members: Golding, Michael C (advisor), Long, Charles R (advisor), Miranda, Rajesh C (committee member), Zhou, Beiyan (committee member).

Subjects/Keywords: Epigenetics; FASD; Histone Modifications

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

APA (6^th Edition):

Veazey, K. J. (2015). An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/156462

Chicago Manual of Style (16^th Edition):

Veazey, Kylee Jordan. “An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders.” 2015. Doctoral Dissertation, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/156462.

MLA Handbook (7^th Edition):

Veazey, Kylee Jordan. “An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders.” 2015. Web. 20 Jan 2021.

Vancouver:

Veazey KJ. An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/156462.

Council of Science Editors:

Veazey KJ. An Epigenetic Basis to the Etiology of Fetal Alcohol Spectrum Disorders. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/156462

Texas A&M University

4. Keith, Ashley Brooke. Consequences of Maternal Nutrient Restriction on Ovine Placental Development.

Degree: PhD, Physiology of Reproduction, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155706

► Maternal nutrient intake and partitioning, uteroplacental blood flow, nutrient transporter activity, and fetoplacental metabolism mediate nutrient delivery to the fetus. Inadequate delivery of nutrients results… (more)

▼ Maternal nutrient intake and partitioning, uteroplacental blood flow, nutrient transporter activity, and fetoplacental metabolism mediate nutrient delivery to the fetus. Inadequate delivery of nutrients results in intrauterine growth restriction (IUGR), a leading cause of neonatal morbidity and mortality. The present studies exploited natural population variance in nutrient-restricted (NR) ewes to identify subpopulations of IUGR and non-IUGR fetuses as subjects for research to elucidate adaptive mechanisms of fetal-placental development. Singleton pregnancies were generated by embryo transfer and assigned to receive either 50% (n=24) or 100% (n=7) of the National Research Council’s (NRC) recommended dietary intake from Day 35 to Day 125 of gestation, at which time ewes were necropsied. Maternal weight did not correlate with fetal weight; therefore, differences in development of the six heaviest (NR non-IUGR) and six lightest (NR IUGR) fetuses from NR ewes, as well as the seven fetuses from control ewes were compared. Mean weights of NR IUGR fetuses (2.8±0.1 kg) were lower (P<0.05) than for control (4.0±0.1 kg) and NR non-IUGR (4.1±0.1 kg) fetuses. The first study investigated potential mechanisms regulating nutrient availability for fetuses. Results indicated that normal fetal growth in a subpopulation of NR ewes is associated with enhanced delivery of a number of amino acids and their metabolites into the fetal circulation, which may at least partially result from up-regulation of expression of amino acid transporter mRNAs in the placentome. The second study elucidated potential physiological mechanisms regulating placental growth and development in ewes having NR IUGR and NR non-IUGR fetuses. Results suggest that placentome morphology and angiogenic growth factor expression varies in response to maternal nutritional challenge during pregnancy and may play critical roles in regulating fetal growth. The third study was conducted to capitalize on natural population variance in NR ewes to identify novel factors regulating placental growth and function. Results suggest that enhanced fetal growth in NR non-IUGR pregnancies is associated with an altered expression of genes related to immune response and function in the placentome. Collectively, results of these studies suggest that enhanced fetal growth in a subset of NR ewes is associated with enhanced expression of select nutrient transporters and angiogenic factors, increased nutrient availability to the fetus, altered placentome morphology, and an altered immune response within the placentomes of those ewes. Advisors/Committee Members: Satterfield, Michael C (advisor), Dunlap, Kathrin A (advisor), Bazer, Fuller W (committee member), Wu, Guoyao (committee member), Golding, Michael C (committee member).

Subjects/Keywords: placenta; nutrient restriction; IUGR; sheep

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APA (6^th Edition):

Keith, A. B. (2015). Consequences of Maternal Nutrient Restriction on Ovine Placental Development. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155706

Chicago Manual of Style (16^th Edition):

Keith, Ashley Brooke. “Consequences of Maternal Nutrient Restriction on Ovine Placental Development.” 2015. Doctoral Dissertation, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/155706.

MLA Handbook (7^th Edition):

Keith, Ashley Brooke. “Consequences of Maternal Nutrient Restriction on Ovine Placental Development.” 2015. Web. 20 Jan 2021.

Vancouver:

Keith AB. Consequences of Maternal Nutrient Restriction on Ovine Placental Development. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/155706.

Council of Science Editors:

Keith AB. Consequences of Maternal Nutrient Restriction on Ovine Placental Development. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155706

Texas A&M University

5. Chang, Cheng-An Richard. The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease.

Degree: PhD, Biomedical Sciences, 2019, Texas A&M University

URL: http://hdl.handle.net/1969.1/188715

► Alcohol is a notorious teratogen and a major driver of both mental and physical defects. Recently, alcohol has been discovered to exert intergenerational effects on… (more)

Subjects/Keywords: Epigenetics

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APA (6^th Edition):

Chang, C. R. (2019). The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/188715

Chicago Manual of Style (16^th Edition):

Chang, Cheng-An Richard. “The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease.” 2019. Doctoral Dissertation, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/188715.

MLA Handbook (7^th Edition):

Chang, Cheng-An Richard. “The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease.” 2019. Web. 20 Jan 2021.

Vancouver:

Chang CR. The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease. [Internet] [Doctoral dissertation]. Texas A&M University; 2019. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/188715.

Council of Science Editors:

Chang CR. The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease. [Doctoral Dissertation]. Texas A&M University; 2019. Available from: http://hdl.handle.net/1969.1/188715

6. Snyder, Matthew D. Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development.

Degree: MS, Biomedical Sciences, 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/157784

► Epigenetic patterns established during early bovine embryogenesis via DNA methylation and histone modification patterns are essential for proper gene expression and embryonic development. Epigenome patterns… (more)

▼ Epigenetic patterns established during early bovine embryogenesis via DNA methylation and histone modification patterns are essential for proper gene expression and embryonic development. Epigenome patterns established during this period, if improperly maintained, can lead to developmental anomalies and may partially explain the lower pregnancy rates of in vitro-produced embryos. We hypothesized that the histone methyltransferase of ASH2L would alter preimplantation development, epigenetic reprogramming, and gene expression profiles in the early bovine embryo. We observed that the depleted and deleted ASH2L embryos developed to the blastocyst stage with suppressed ASH2L having comparable development rates with its respective control (31.3 ± 2.0%, n = 466 v. 34.8 ± 1.9%, n = 418). To see if errors were in the chromatin structure at the blastocyst stage, DNA methylation and histone modifications were examined to further explain the role of ASH2L during embryonic development. Blastocysts from each treatment (N = 601) were fixed and prepared for immunocytochemistry following standard laboratory protocol. Our findings show ASH2L may play a role in DNA methylation by decreasing 5mc and 5hmc conversion, which is a key event during early embryonic development. Suppression of ASH2L also alters global levels of H3H4me3 and H3K27me3 (p<0.001), which may lead to transcription aberrations. RNA-seq showed altered gene expression profiles in 407 genes in the morphologically comparable Day 17 conceptus (p<0.05). Closer examination showed that there is altered mesenchymal stem cell differentiation present in the Day 17 conceptuses. Analysis of ASH2L shows to not have a detrimental effect during preimplantation development but altered chromatin status and gene expression profiles suggest that ASH2L could play a vital role later in development. Advisors/Committee Members: Long, Charles R (advisor), Westhusin, Mark E (committee member), Golding, Michael C (committee member), Satterfield, Carey (committee member).

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APA (6^th Edition):

Snyder, M. D. (2016). Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157784

Chicago Manual of Style (16^th Edition):

Snyder, Matthew D. “Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development.” 2016. Masters Thesis, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/157784.

MLA Handbook (7^th Edition):

Snyder, Matthew D. “Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development.” 2016. Web. 20 Jan 2021.

Vancouver:

Snyder MD. Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development. [Internet] [Masters thesis]. Texas A&M University; 2016. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/157784.

Council of Science Editors:

Snyder MD. Analysis of the Histone Methyltransferase ASH2L via RNA Interference and CRISPR-Cas9 during Bovine Early Embryonic Development. [Masters Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157784

7. Skiles, William Mark. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.

Degree: PhD, Biomedical Sciences, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/173200

► In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how… (more)

▼ In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how environmental exposures influence the long-term health of an organism. Chemical pollutants, dietary deficiencies, embryonic stress and multiple other external factors have all demonstrated long-lasting effects upon development, metabolism, and health even after transient exposures. The mechanisms by which these exposures can impact development far beyond the period of exposure remain largely unknown. To gain better insight into the developmental origins of both birth defects and disease, we must better understand how environmental exposures alter development. In this work, we will examine the capacity of the environment to impact chromatin states, and then determine whether these changes are heritable; and are thus potentially causal in the development of disease. This is an important question due to the recent recognition that aberrant chromatin states can lead to pathological patterns of gene expression, a circumstance commonly referred to as “epimutations”. Dysregulation of gene expression patterns during development have been shown to cause a multitude of irregular phenotypes in offspring and lifelong disorders in mature organisms. This altered chromatin state, coined an epimutation by Dr. Emma Whitelaw, is important due to the mutation not being in the genetic code itself, but in the way DNA regulatory regions are packaged within the chromatin template, and thus accessed by the protein factors directing gene transcription. The body of work presented here will examine the ability of common environmental exposures to modulate chromatin structure. We will examine these changes over time in an effort to better understand the inheritance of epigenetic change. Secondly, we will measure whether environmentally induced alterations in chromatin structure within the germline persist, and are heritable. These questions are all relevant to better understanding the developmental origins of disease. Advisors/Committee Members: Golding, Michael C (advisor), Long, Charles R (advisor), Seabury, Christopher M (committee member), Johnson, Natalie M (committee member).

Subjects/Keywords: oxidative stress; assisted reproductive technologies; genomic imprinting; histone demethylase; TET; DNMT; DNA methylation; epigenetics; developmental programming; DOHAD; birth defect; epigenetics; preconception; sperm

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APA (6^th Edition):

Skiles, W. M. (2017). Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173200

Chicago Manual of Style (16^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Doctoral Dissertation, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/173200.

MLA Handbook (7^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Web. 20 Jan 2021.

Vancouver:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/173200.

Council of Science Editors:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/173200

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