subject:(DNA methylation)

University of Georgia

1. Taniguchi, Yu. The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2.

Degree: BS, Biochemistry and Molecular Biology, 2010, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/taniguchi_yu_201005_bs

► Histone modifications, DNA methylation, and nucleosome occupancy are known to play an important role in regulation of transcription. The purpose of the study was to… (more)

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Taniguchi, Y. (2010). The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2. (Thesis). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/taniguchi_yu_201005_bs

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):

Taniguchi, Yu. “The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2.” 2010. Thesis, University of Georgia. Accessed February 19, 2020. http://purl.galileo.usg.edu/uga_etd/taniguchi_yu_201005_bs.

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

MLA Handbook (7^th Edition):

Taniguchi, Yu. “The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2.” 2010. Web. 19 Feb 2020.

Vancouver:

Taniguchi Y. The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2. [Internet] [Thesis]. University of Georgia; 2010. [cited 2020 Feb 19]. Available from: http://purl.galileo.usg.edu/uga_etd/taniguchi_yu_201005_bs.

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

Council of Science Editors:

Taniguchi Y. The relationship between DNA methylation and nucleosome occupancy involving in a transcriptional activity of SOX2. [Thesis]. University of Georgia; 2010. Available from: http://purl.galileo.usg.edu/uga_etd/taniguchi_yu_201005_bs

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

University of Hong Kong

2. Kwan, Chun-kit, Peter. Development and application of a single mouse embryo DNA methylation-detection assay.

Degree: M. Phil., 2014, University of Hong Kong

URL: Kwan, C. P. [關駿傑]. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5194756 ; http://dx.doi.org/10.5353/th_b5194756 ; http://hdl.handle.net/10722/197532

► During preimplantation embryonic development, imprinting genes are susceptible to methylation changes by artificial manipulation, which may lead to developmental abnormalities. In addition, environmental endocrine disruptors… (more)

▼ During preimplantation embryonic development, imprinting genes are susceptible to methylation changes by artificial manipulation, which may lead to developmental abnormalities. In addition, environmental endocrine disruptors (EDs) in everyday household products are also found to perturb fertility development and cause epigenetic aberrations. While embryo supply is scarce and conventional epigenetic studies require embryos in vast amount, an assay was developed in this study to examine the methylation statuses of imprinting genes using DNA from single mouse blastocysts cultured in-vitro or exposed to EDs. Promoter CpG methylation patterns of three imprinting genes, small nuclear ribonucleoprotein polypeptide N (SNRPN), paternally expressed 3 (Peg3), and potassium voltage-gated channel 1 overlapping transcript 1 (Kcnq1ot1), were examined from genomic DNA of a single mouse blastocyst. The genomic DNA was isolated and treated with bisulfite modification to preserve the methylation statuses. Afterwards, the DNA was subjected to whole genome amplification (WGA). Methylation-specific polymerase chain reaction (methyl-PCR) was performed with allele-specific primers; the amplicons were cloned and sequenced. CpG methylations in SNRPN, Peg3 and Kcnq1ot1 showed no statistical significant difference (P>0.05; Mann Whitney U test) in both parental alleles between a single genomic-amplified blastocyst and 20 non-amplified blastocysts, indicating no artifact was being introduced during the WGA procedure. Using the assay, it was revealed that blastocysts cultured in-vitro expressed slight but nonsignificant deviation in methylation rates to both parental alleles of SNRPN and Kcnq1ot1 except in single blastocysts, which displayed significant loss in maternal methylation on SNRPN upon culturing. On the other hand, paternal methylation profile of Peg3 appeared unaffected, suggesting resistance to methylation perturbations induced by in-vitro culturing. Despite that there was no significant difference in overall methylation rates between in-vivo or in-vitro developed blastocysts, certain CpG residues appeared to displayed significant loss of methylation (LOM) or gain of methylation (GOM) induced by in-vitro culture in all three genes being studied. Furthermore, using the developed, assay the epigenetic effects of three endocrine disruptors, simazine, propiconazole, and cadmium chloride (CdCl2) on in-vitro cultured single blastocysts were revealed. When compared to blastocysts cultured with KSOM+AA medium as controls, CdCl2-treated blastocysts displayed the most methylation aberrations in both alleles and within particular CpG residues, possibly due to its dual effect in both hypermethylation and hypomethylation across the methylome. Both simazine- and propiconazole -treated blastocysts displayed overall methylation significant defects were observed within particular CpG residues. Overall, the assay used in this study allowed the comprehensive investigation of methylome from the DNA extracted from a single blastocyst.defects resembled to…

Subjects/Keywords: DNA - Methylation

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APA (6^th Edition):

Kwan, Chun-kit, P. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Masters Thesis). University of Hong Kong. Retrieved from Kwan, C. P. [關駿傑]. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5194756 ; http://dx.doi.org/10.5353/th_b5194756 ; http://hdl.handle.net/10722/197532

Chicago Manual of Style (16^th Edition):

Kwan, Chun-kit, Peter. “Development and application of a single mouse embryo DNA methylation-detection assay.” 2014. Masters Thesis, University of Hong Kong. Accessed February 19, 2020. Kwan, C. P. [關駿傑]. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5194756 ; http://dx.doi.org/10.5353/th_b5194756 ; http://hdl.handle.net/10722/197532.

MLA Handbook (7^th Edition):

Kwan, Chun-kit, Peter. “Development and application of a single mouse embryo DNA methylation-detection assay.” 2014. Web. 19 Feb 2020.

Vancouver:

Kwan, Chun-kit P. Development and application of a single mouse embryo DNA methylation-detection assay. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2020 Feb 19]. Available from: Kwan, C. P. [關駿傑]. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5194756 ; http://dx.doi.org/10.5353/th_b5194756 ; http://hdl.handle.net/10722/197532.

Council of Science Editors:

Kwan, Chun-kit P. Development and application of a single mouse embryo DNA methylation-detection assay. [Masters Thesis]. University of Hong Kong; 2014. Available from: Kwan, C. P. [關駿傑]. (2014). Development and application of a single mouse embryo DNA methylation-detection assay. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5194756 ; http://dx.doi.org/10.5353/th_b5194756 ; http://hdl.handle.net/10722/197532

3. Accomando, William Paul. Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue.

Degree: PhD, Pathobiology, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320602/

► Different types of human cells, defined by function and morphology, are typically detected and enumerated in complex mixtures using a variety of physical, optical and… (more)

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Accomando, W. P. (2013). Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320602/

Chicago Manual of Style (16^th Edition):

Accomando, William Paul. “Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue.” 2013. Doctoral Dissertation, Brown University. Accessed February 19, 2020. https://repository.library.brown.edu/studio/item/bdr:320602/.

MLA Handbook (7^th Edition):

Accomando, William Paul. “Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue.” 2013. Web. 19 Feb 2020.

Vancouver:

Accomando WP. Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2020 Feb 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:320602/.

Council of Science Editors:

Accomando WP. Epigenetic Biomarkers for the Detection and Quantification of Human Leukocytes in Blood and Tissue. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320602/

4. Smith, Ashley A. Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma.

Degree: PhD, Pathobiology, 2014, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:386178/

► Gliomas are a family of extremely aggressive brain cancers, which, despite current treatment options, have poor prognoses. There are distinct subtypes of gliomas, and accurately… (more)

▼ Gliomas are a family of extremely aggressive brain cancers, which, despite current treatment options, have poor prognoses. There are distinct subtypes of gliomas, and accurately identifying these is critical for diagnosis and management. Often, the pathologic diagnosis of these subtypes is difficult, and research is underway to discover novel biomarkers that aid in accurate subtype identification and prognostication. This thesis focuses on the joint analysis of DNA methylation profiles with somatic mutation and gene expression data in glioma, assessing the nature of their association with each other and, subsequently, with histology and disease outcome. The ultimate goal is to develop potential prognostic biomarkers of the disease. DNA methylation was determined for several different grades and histologies of glioma in addition to non-brain-tumor controls. The same samples were sequenced for IDH1/2 mutations. We, and others, discovered an IDH hypermethylator phenotype, showing a tight association between the occurrence of IDH mutation and hypermethylation. This phenotype had a higher prevalence in low-grade and secondary gliomas. Besides mutation, DNA methylation is also associated with other somatic alterations, which can alter gene expression. To better understand how DNA methylation and gene expression drive glioma, we used an integrative bioinformatics approach; our goal was to investigate DNA methylation that modulates gene expression as well as independent DNA methylation (methylation that may exert its phenotypic effects through alternative mechanisms), assessing the nature of their association with disease survival. Our model supports the existing theory that DNA methylation can work through gene expression to influence survival outcome but also suggests that DNA methylation can work alone or through alternative mechanisms to influence glioma outcome. In addition, our approach offers an alternative method of biomarker discovery, which could potentially be used for diagnostic and therapeutic purposes. Overall, this work supports the hypothesis that somatic mutations are not solely responsible for the glioma phenotype. Epigenetics, particularly DNA methylation, is also important in both the genesis and outcome of the disease. Furthermore, our model provides an alternative approach for biomarker discovery that may also be applicable to cancers other than glioma. Advisors/Committee Members: Kelsey, Karl (Director), Marsit, Carmen (Reader), Houseman, E. Andres (Reader), Huang, Yen-Tsung (Reader), Wiencke, John (Reader).

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Smith, A. A. (2014). Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:386178/

Chicago Manual of Style (16^th Edition):

Smith, Ashley A. “Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma.” 2014. Doctoral Dissertation, Brown University. Accessed February 19, 2020. https://repository.library.brown.edu/studio/item/bdr:386178/.

MLA Handbook (7^th Edition):

Smith, Ashley A. “Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma.” 2014. Web. 19 Feb 2020.

Vancouver:

Smith AA. Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2020 Feb 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:386178/.

Council of Science Editors:

Smith AA. Integration of Genetic and Epigenetic Alterations in the Discovery of Molecular Drivers of Malignancy in Glioma. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:386178/

5. Cash, Haley L. DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease.

Degree: PhD, Pathobiology, 2011, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:11329/

► Non-communicable diseases have recently surpassed communicable diseases as the number one cause of death globally. These conditions not only lead to increased rates of mortality,… (more)

▼ Non-communicable diseases have recently surpassed communicable diseases as the number one cause of death globally. These conditions not only lead to increased rates of mortality, but also contribute to global disability that can greatly impede development. Although many environmental and genetic risk factors have been associated with these conditions, epigenetic mechanisms have yet to be properly explored in these diseases. This thesis aimed to further understand the relationships between DNA methylation and environmental factors as well as genetic factors in relation to various non-communicable diseases. When examining the relationships between LINE-1 methylation, bladder cancer, and risk factors in the Shanghai Bladder Cancer Study, LINE-1 hypomethylation was found to be significantly associated with increased risk of bladder cancer among non-smokers; risk was greatest among these individuals with null glutathione-s-transferase genoytypes. In this study we also found that CYP1A2 phenotype among smokers, cruciferous vegetable intake, and glutathione-s-transferase genotypes significantly influenced LINE-1 methylation among controls. Additionally, men had significantly higher levels of LINE-1 methylation than women. This LINE-1 gender difference was also observed in The Samoan Family Study of Overweight and Obese when LINE-1 methylation was measured in this population. Additionally, LINE-1 methylation was found to be negatively associated with age as well as HDL in men; whereas insulin and testosterone levels were associated with LINE-1 methylation among women. Finally, the effects of bladder cancer risk genetic variants within the PSCA gene (rs2294008) on CpG methylation was evaluated by examining array based DNA methylation profiles. Upon investigation, there were not array-wide methylation associations with variation; however, methylation of a CpG within the PSCA gene was significantly associated with SNP status in a dose-response fashion, in which there was a positive relationship between risk allele quantity and CpG methylation. Overall, this work demonstrates the importance of DNA methylation in non-communicable diseases. Additionally, this work suggests that complex relationships exist between environmental factors, genetics, and epigenetics, advocating the need for further investigations in order to more effectively understand the role of DNA methylation in non-communicable disease. Advisors/Committee Members: Kelsey, Karl (Director), McGarvey, Stephen (Reader), Marsit, Carmen (Reader), Houseman, E (Reader), Karagas, Margaret (Reader).

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Cash, H. L. (2011). DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:11329/

Chicago Manual of Style (16^th Edition):

Cash, Haley L. “DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease.” 2011. Doctoral Dissertation, Brown University. Accessed February 19, 2020. https://repository.library.brown.edu/studio/item/bdr:11329/.

MLA Handbook (7^th Edition):

Cash, Haley L. “DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease.” 2011. Web. 19 Feb 2020.

Vancouver:

Cash HL. DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease. [Internet] [Doctoral dissertation]. Brown University; 2011. [cited 2020 Feb 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:11329/.

Council of Science Editors:

Cash HL. DNA Methylation of Repeat Regions in Human Cancer and Metabolic Disease. [Doctoral Dissertation]. Brown University; 2011. Available from: https://repository.library.brown.edu/studio/item/bdr:11329/

University of Southern California

6. Triche, Timothy J., Jr. Preprocessing and analysis of DNA methylation microarrays.

Degree: PhD, Statistical Genetics and Genetic Epidemiology, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/298429/rec/5203

► In the first chapter of this dissertation, I review the importance of cytosine methylation in vertebrate genomes. In the second chapter, I present methods which… (more)

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Triche, Timothy J., J. (2013). Preprocessing and analysis of DNA methylation microarrays. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/298429/rec/5203

Chicago Manual of Style (16^th Edition):

Triche, Timothy J., Jr. “Preprocessing and analysis of DNA methylation microarrays.” 2013. Doctoral Dissertation, University of Southern California. Accessed February 19, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/298429/rec/5203.

MLA Handbook (7^th Edition):

Triche, Timothy J., Jr. “Preprocessing and analysis of DNA methylation microarrays.” 2013. Web. 19 Feb 2020.

Vancouver:

Triche, Timothy J. J. Preprocessing and analysis of DNA methylation microarrays. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2020 Feb 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/298429/rec/5203.

Council of Science Editors:

Triche, Timothy J. J. Preprocessing and analysis of DNA methylation microarrays. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/298429/rec/5203

Wake Forest University

7. Cammarata, Michael Wesley. DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort.

Degree: 2015, Wake Forest University

URL: http://hdl.handle.net/10339/57275

Background: P2Y12 receptor is the target for thienopyridine mediated platelet inhibition. Epigenetic factors, including DNA methylation could influence gene expression and subsequent in vitro and clinical response to thienopyridine therapy. Our aim was to determine the relationships between DNA methylation at cis acting CpG sites and P2RY12 gene expression.

Subjects/Keywords: DNA Methylation

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APA (6^th Edition):

Cammarata, M. W. (2015). DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/57275

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):

Cammarata, Michael Wesley. “DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort.” 2015. Thesis, Wake Forest University. Accessed February 19, 2020. http://hdl.handle.net/10339/57275.

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

MLA Handbook (7^th Edition):

Cammarata, Michael Wesley. “DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort.” 2015. Web. 19 Feb 2020.

Vancouver:

Cammarata MW. DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort. [Internet] [Thesis]. Wake Forest University; 2015. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10339/57275.

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

Council of Science Editors:

Cammarata MW. DNA Methylation and Gene Expression of P2RY12 in a Multi-Ethnic Cohort. [Thesis]. Wake Forest University; 2015. Available from: http://hdl.handle.net/10339/57275

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

University of Edinburgh

8. Masalmeh, Roza Hussein Ali. Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells.

Degree: PhD, 2019, University of Edinburgh

URL: http://hdl.handle.net/1842/35826

► Disruption of DNA methylation patterns is a primary hallmark of cancer. One main disruption is CpG islands (CGIs) aberrant hypermethylation which is associated with transcriptional… (more)

▼ Disruption of DNA methylation patterns is a primary hallmark of cancer. One main disruption is CpG islands (CGIs) aberrant hypermethylation which is associated with transcriptional repression of tumour suppressor genes such as BRCA1, MLH1, and CDKN2A (p16/ARF). However, the mechanism(s) underpinning this process are still unknown. One hypothesis is that high de novo methylation activity is targeted to CGIs that get aberrantly methylated in cancer. To investigate this, I used human colorectal cancer cell line (HCT116) as a model. Firstly, I have ectopically integrated representative aberrantly methylated CGIs randomly into the genome and assessed their methylation at ectopic loci. I show that integrated CGIs rarely gained methylation at ectopic locations. This suggested that the sequence doesn't program CGIs aberrant methylation at ectopic loci in HCT116 and that low de novo methylation is targeted to aberrantly methylated CGIs. Next, I wanted to confirm this result by integrating CGIs at a chosen genomic loci in order to exclude any effects from the CGI position on its methylation status. This was performed by recombinase mediated cassette exchange (RMCE). Successful targeting of a RMCE cassette to the desired chromosomal locus was achieved. However, isolating clonal cell lines with integrated CGIs was technically infeasible due to difficulty in using the thymidine kinase selection in HCT116. In order to investigate which CGIs have higher de novo methylation in HCT116 on a genome wide level, I restored DNMT3B expression in DNMTA1/DNMT3B double knockout (DKO) of HCT116. In agreement with previous reports, DNMT3B showed higher de novo methylation activity at CGIs overlapping H3K36me3. Most importantly, aberrantly methylated CGIs showed ~ 78.5% less methylation gain compared to normally methylated CGIs. To confirm results from this experiment, I treated HCT116 with 5-Aza-2'-deoxycytidine and then allowed cells to recover methylation. The rate of methylation recovery of CGIs was assessed. This showed that aberrantly methylated CGIs recover slower than normally methylated CGIs, confirming that lower de novo methylation is targeted to aberrantly methylated CGIs compared to normally methylated ones. The work carried out during the course of this thesis provides novel insights into the process of de novo methylating CGIs in cancer on a genome wide level. It suggests that low levels, rather than high levels, of methylation are targeted to aberrantly methylated CGIs in colorectal tumours.

Subjects/Keywords: DNA methylation; DNMT3B; methylation; HCT116

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APA (6^th Edition):

Masalmeh, R. H. A. (2019). Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/35826

Chicago Manual of Style (16^th Edition):

Masalmeh, Roza Hussein Ali. “Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells.” 2019. Doctoral Dissertation, University of Edinburgh. Accessed February 19, 2020. http://hdl.handle.net/1842/35826.

MLA Handbook (7^th Edition):

Masalmeh, Roza Hussein Ali. “Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells.” 2019. Web. 19 Feb 2020.

Vancouver:

Masalmeh RHA. Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells. [Internet] [Doctoral dissertation]. University of Edinburgh; 2019. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1842/35826.

Council of Science Editors:

Masalmeh RHA. Low levels of methylation are targeted to aberrantly methylated CGIs in human colorectal cancer cells. [Doctoral Dissertation]. University of Edinburgh; 2019. Available from: http://hdl.handle.net/1842/35826

University of Hawaii – Manoa

9. Song, Min-Ae. Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100485

►

Ph.D. University of Hawaii at Manoa 2014.

My research project focused on the identification of aberrant epigenetic changes via non-coding RNAs and DNA methylation in… (more)

▼

Ph.D. University of Hawaii at Manoa 2014.

My research project focused on the identification of aberrant epigenetic changes via non-coding RNAs and DNA methylation in MSS/CIMP-negative colon cancer, the major subtype. DNA methylation is the most well studied epigenetic event, while non-coding RNA-mediated transcriptional silencing has also an important role in cancer. My first aim was to profile microRNAs and their potential target genes in colon cancer by a study of 10 paired normal and tumor colon tissues using data from Next Generation Sequencing and Exon arrays. Nineteen miRNAs, including 6 previously colon cancer associated and 13 not previously implicated, were found aberrantly expressed in the tumor tissues. Thirty-six colon cancer related genes were significantly correlated to the expression levels of the identified miRNAs and 'Wnt/beta-catenin Signaling' was identified as the top canonical pathway for these target genes. My second aim was to identify small and long novel non-coding RNAs at the 8q24 region which contains one of the most relevant colon cancer risk variants, SNP rs6983267. Thirty-two pre-miRNAs were identified In Silico by two algorithms, but none of them were verified in further studies. However, a novel long non-coding RNA spanning the rs6983267 was recently identified, and significantly elevated expression levels were observed in 23 colon tumor tissues in our sample set. Also, one known miRNA in a cluster 400 kb away from the risk SNP showed genotype dependent expression patterns. My last aim was to elucidate the landscape of genome-wide DNA methylation in colon cancer. General hypomethylation was observed, concentrating in the intergenic regions and gene bodies, while hypermethylation was observed in promoter regions, N_Shores and CpG islands. Differentially methylated CpGs were enriched in genes with roles in cancer and gastrointestinal disease. Observations in imprinted genes suggest a more widespread dysregulation of imprinting in colon cancer than previously reported. The findings of epigenetic alterations in colon cancer will hopefully contribute to a better understanding of these aberrant events: how they are related to colon cancer development and progression, while these findings may also lead to discovery of new biomarkers that can be utilized in patient diagnosis, stratification and the follow-up of the treatment.

Subjects/Keywords: RNAs; DNA methylation

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APA (6^th Edition):

Song, M. (2015). Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100485

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):

Song, Min-Ae. “Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer.” 2015. Thesis, University of Hawaii – Manoa. Accessed February 19, 2020. http://hdl.handle.net/10125/100485.

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

MLA Handbook (7^th Edition):

Song, Min-Ae. “Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer.” 2015. Web. 19 Feb 2020.

Vancouver:

Song M. Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10125/100485.

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

Council of Science Editors:

Song M. Identification of aberrant epigenetic events in MSS/CIMP-negative colon cancer. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100485

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

University of Hong Kong

10. Li, Tao. Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1.

Degree: M. Phil., 2016, University of Hong Kong

URL: http://hdl.handle.net/10722/240653

►

DNA methylation is a crucial epigenetic modification and functions as a key factor in controlling gene expression and mammalian development. The DNA methyltransferase DNMT1 is… (more)

Subjects/Keywords: Ubiquitin; DNA - Methylation

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APA (6^th Edition):

Li, T. (2016). Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/240653

Chicago Manual of Style (16^th Edition):

Li, Tao. “Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1.” 2016. Masters Thesis, University of Hong Kong. Accessed February 19, 2020. http://hdl.handle.net/10722/240653.

MLA Handbook (7^th Edition):

Li, Tao. “Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1.” 2016. Web. 19 Feb 2020.

Vancouver:

Li T. Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1. [Internet] [Masters thesis]. University of Hong Kong; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10722/240653.

Council of Science Editors:

Li T. Structural and mechanistic insights into UHRF1-coordinated maintenance DNA methylation by DNMT1. [Masters Thesis]. University of Hong Kong; 2016. Available from: http://hdl.handle.net/10722/240653

University of Western Australia

11. Ang, Sophia Pei Woon. DNA methylation in colorectal cancer.

Degree: PhD, 2009, University of Western Australia

URL: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=14979&local_base=GEN01-INS01

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[Truncated abstract] De novo methylation of CpG islands in gene promoter regions is an alternative gene silencing mechanism that contributes to the development and progression… (more)

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[Truncated abstract] De novo methylation of CpG islands in gene promoter regions is an alternative gene silencing mechanism that contributes to the development and progression of colorectal cancer (CRC). CRCs that exhibit widespread hypermethylation of gene promoters are referred to as having the CpG island methylator phenotype (CIMP). To improve our understanding of the CIMP+ subgroup of CRC, the first aim of this research was to address one of the technical limitations of methylation analysis by developing a quality control system for sample DNA (Chapter 3). A ridge-regression approach was then devised in an attempt to identify CpG loci whose methylation status was predictive of gene expression (Chapter 4). Comprehensive methylation profiling was used to further characterise CRC based on unbiased analysis of DNA methylation levels (Chapter 5). Finally, CIMP+ was evaluated in a large series of young CRC patients with the longer term aim of identifying possible familial cases of this CRC subtype (Chapter 6). A growing number of studies have shown that aberrant tumour DNA methylation may represent a promising molecular diagnostic, prognostic and predictive marker. This has generated the need for accurate quality control systems for the analysis of DNA methylation in clinical specimens. An adequate amount of DNA after bisulfite treatment and the subsequent availability of sufficient target molecules for PCR based methylation analyses are critical for ensuring accurate quantification. In Chapter 3, experiments that tested multiple extractions, processing, analytical methods and sample types were conducted. These demonstrated that cycle threshold (Ct) value was superior to spectrophotometric analysis for predicting the suitability of DNA for methylation analyses. The potential benefits of this approach are improvements in the reproducibility of methylation analysis and in sample management. Since DNA hypermethylation of promoter regions is involved in the

transcriptional regulation of many genes, it is widely used as a surrogate marker for gene expression. However, most existing DNA methylation assays have not been correlated with corresponding gene expression. In Chapter 4, a ridge-regression model was developed with the aim of identifying CpG loci that were predictive of RNA levels for the RUNX3 and DPYD genes in CRC. The model was developed using methylation and RNA expression data obtained in a panel of CRC cell lines. When tested in primary CRC, the methylation status of the candidate CpG sites failed to predict RNA expression. These findings suggest that quantitative and qualitative differences between training and validation samples should be considered when constructing models for the prediction of methylation-dependent RNA expression. The use of an unbiased and comprehensive methylation profiling approach described in Chapter 5 identified three CIMP subgroups in CRC associated with distinct clinicopathological and molecular characteristics. BRAF and KRAS mutations were positively associated with the CIMP-high…

Subjects/Keywords: Colon (Anatomy); DNA; DNA; DNA; Methylation; Rectum; DNA methylation; Colorectal cancer

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

APA (6^th Edition):

Ang, S. P. W. (2009). DNA methylation in colorectal cancer. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=14979&local_base=GEN01-INS01

Chicago Manual of Style (16^th Edition):

Ang, Sophia Pei Woon. “DNA methylation in colorectal cancer.” 2009. Doctoral Dissertation, University of Western Australia. Accessed February 19, 2020. http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=14979&local_base=GEN01-INS01.

MLA Handbook (7^th Edition):

Ang, Sophia Pei Woon. “DNA methylation in colorectal cancer.” 2009. Web. 19 Feb 2020.

Vancouver:

Ang SPW. DNA methylation in colorectal cancer. [Internet] [Doctoral dissertation]. University of Western Australia; 2009. [cited 2020 Feb 19]. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=14979&local_base=GEN01-INS01.

Council of Science Editors:

Ang SPW. DNA methylation in colorectal cancer. [Doctoral Dissertation]. University of Western Australia; 2009. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=14979&local_base=GEN01-INS01

University of Edinburgh

12. Termanis, Ausma. Regulators of DNA methylation in mammalian cells.

Degree: PhD, 2013, University of Edinburgh

URL: http://hdl.handle.net/1842/11749

► Although the many cells within a mammal share the same DNA sequence, their gene expression programmes are highly heterogeneous, and their functions correspondingly diverse. This… (more)

Subjects/Keywords: 572.8; epigenetics; DNA methylation; X chromosome methylation

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APA (6^th Edition):

Termanis, A. (2013). Regulators of DNA methylation in mammalian cells. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/11749

Chicago Manual of Style (16^th Edition):

Termanis, Ausma. “Regulators of DNA methylation in mammalian cells.” 2013. Doctoral Dissertation, University of Edinburgh. Accessed February 19, 2020. http://hdl.handle.net/1842/11749.

MLA Handbook (7^th Edition):

Termanis, Ausma. “Regulators of DNA methylation in mammalian cells.” 2013. Web. 19 Feb 2020.

Vancouver:

Termanis A. Regulators of DNA methylation in mammalian cells. [Internet] [Doctoral dissertation]. University of Edinburgh; 2013. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1842/11749.

Council of Science Editors:

Termanis A. Regulators of DNA methylation in mammalian cells. [Doctoral Dissertation]. University of Edinburgh; 2013. Available from: http://hdl.handle.net/1842/11749

University of Hong Kong

13. Wong, Kin-yiu. Correlation of TSPY expression level and its promoter methylation status in liver cancer.

Degree: Master of Medical Sciences, 2016, University of Hong Kong

URL: http://hdl.handle.net/10722/237202

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Background: Hepatocellular carcinoma (HCC) is the 6th most common cancer and the 2nd leading cause of cancer deaths globally. TSPY (Testis-specific protein Y-encoded) is normally… (more)

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Background: Hepatocellular carcinoma (HCC) is the 6th most common cancer and the 2nd leading cause of cancer deaths globally. TSPY (Testis-specific protein Y-encoded) is normally expressed in testis. Recent studies demonstrated the presence of TSPY transcript in some tumors including HCC, suggesting its tumorigenic role in hepatocarcinogenesis. Methylation status in other cancers was investigated previously, showing TSPY expression might be regulated by DNA methylation. This prompts us to interrogate the potential epigenetic regulation of TSPY expression in HCC. In this study, we determined the methylation status of TSPY promoter site in clinical samples and attempted to correlate it with mRNA expression. Methods: Expression of TSPY was examined using quantitative real-time PCR (qPCR). HCC Cell line Huh7 and immortalized normal liver cell line MIHA, which showed low endogenous TSPY expression, were treated with DNA methyltransferase inhibitor 5-Aza-2'-Deoxycytidine (5-aza). qPCR was performed to compare TSPY expression levels before and after treatment. Huh7 was selected to analyze the methylation status in promoter site of TSPY using Bisulfite genomic sequencing (BGS). Methylation-specific PCR (MS-PCR) of the selected CpG island region was performed in 12 HCC clinical samples to evaluate the methylation status in tumor as compared with the non-tumoral counterpart. Methylation status was then correlated with expression level of TPSY in the clinical samples. Results: By qPCR, upregulation, downregulation and no significant difference of TSPY mRNA expression (tumor compared with non-tumorous tissues) was found in 40% (10 of 25) cases, 36% (9 of 25) cases and 24% (6 of 25) cases respectively. By Western blotting, low endogenous level of TSPY protein expression was found in Huh7 and MIHA cell lines. Subsequent qPCR of these two 5-aza-treated cell lines showed restoration of TSPY mRNA expression. Four potential CpG islands were identified through online programme MethPrimer and one was chosen in this study. BGS results showed a 48.3% probability of methylation in 3 clones of Huh7 cells treated with 2μM 5-aza for 3 days. For MS-PCR result, “hypermethylation”, “hypomethylation” and “no significant differences” status were found in 41.7% (5 of 12), 41.7% (5 of 12) and 16.7% (2 of 12) cases respectively. Correlation between TSPY mRNA expression and promoter site methylation status showed a “concordance” in 33.3% in the clinical samples (4 of 12 cases). Conclusions: Our findings suggested that promoter site methylation status might not be a major regulatory mechanism on the expression of TSPY in HCC. Further studies are recommended to consolidate the findings.

published_or_final_version

Pathology

Master

Master of Medical Sciences

Subjects/Keywords: Nucleoproteins; Liver - Cancer; DNA - Methylation

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

APA (6^th Edition):

Wong, K. (2016). Correlation of TSPY expression level and its promoter methylation status in liver cancer. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/237202

Chicago Manual of Style (16^th Edition):

Wong, Kin-yiu. “Correlation of TSPY expression level and its promoter methylation status in liver cancer.” 2016. Masters Thesis, University of Hong Kong. Accessed February 19, 2020. http://hdl.handle.net/10722/237202.

MLA Handbook (7^th Edition):

Wong, Kin-yiu. “Correlation of TSPY expression level and its promoter methylation status in liver cancer.” 2016. Web. 19 Feb 2020.

Vancouver:

Wong K. Correlation of TSPY expression level and its promoter methylation status in liver cancer. [Internet] [Masters thesis]. University of Hong Kong; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10722/237202.

Council of Science Editors:

Wong K. Correlation of TSPY expression level and its promoter methylation status in liver cancer. [Masters Thesis]. University of Hong Kong; 2016. Available from: http://hdl.handle.net/10722/237202

University of Hong Kong

14. Yeung, Kit-san. The use of genome-wide DNA methylation microarray to study both the common and rare diseases.

Degree: M. Phil., 2014, University of Hong Kong

URL: Yeung, K. [楊傑燊]. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5334844 ; http://dx.doi.org/10.5353/th_b5334844 ; http://hdl.handle.net/10722/220770

► DNA methylation plays many important roles in human physiology such as imprinting and X chromosome inactivation (XCI), and therefore disruption in DNA methylation can lead… (more)

Subjects/Keywords: DNA - Methylation; Medical genetics

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APA (6^th Edition):

Yeung, K. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Masters Thesis). University of Hong Kong. Retrieved from Yeung, K. [楊傑燊]. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5334844 ; http://dx.doi.org/10.5353/th_b5334844 ; http://hdl.handle.net/10722/220770

Chicago Manual of Style (16^th Edition):

Yeung, Kit-san. “The use of genome-wide DNA methylation microarray to study both the common and rare diseases.” 2014. Masters Thesis, University of Hong Kong. Accessed February 19, 2020. Yeung, K. [楊傑燊]. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5334844 ; http://dx.doi.org/10.5353/th_b5334844 ; http://hdl.handle.net/10722/220770.

MLA Handbook (7^th Edition):

Yeung, Kit-san. “The use of genome-wide DNA methylation microarray to study both the common and rare diseases.” 2014. Web. 19 Feb 2020.

Vancouver:

Yeung K. The use of genome-wide DNA methylation microarray to study both the common and rare diseases. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2020 Feb 19]. Available from: Yeung, K. [楊傑燊]. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5334844 ; http://dx.doi.org/10.5353/th_b5334844 ; http://hdl.handle.net/10722/220770.

Council of Science Editors:

Yeung K. The use of genome-wide DNA methylation microarray to study both the common and rare diseases. [Masters Thesis]. University of Hong Kong; 2014. Available from: Yeung, K. [楊傑燊]. (2014). The use of genome-wide DNA methylation microarray to study both the common and rare diseases. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5334844 ; http://dx.doi.org/10.5353/th_b5334844 ; http://hdl.handle.net/10722/220770

University of Newcastle

15. Barzideh, Jaleh. Epigenetic modification in human male germ line.

Degree: MPhil, 2010, University of Newcastle

URL: http://hdl.handle.net/1959.13/923302

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Masters Research - Master of Philosophy (MPhil)

The purpose of this study was to examine the methylation status of human sperm DNA in relation to… (more)

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Masters Research - Master of Philosophy (MPhil)

The purpose of this study was to examine the methylation status of human sperm DNA in relation to the functional competence of these cells. In order to achieve this aim discontinuous Percoll gradient density centrifugation was used to generate sperm populations that were either normal (high-density Percoll fraction) or functionally impaired (low density Percoll fraction). The methylation status of these cells was then examined using HPLC, immunocytochemistry or flow cytometry and ultimately correlated with additional markers reflecting the tendency of these cells to default to an intrinsic apoptotic pathway. The results of this study suggest that the mitochondrial genome is heavily methylated during spermatogenesis possibly as a means of suppressing expression of the paternal mitochondrial genome following fertilization. Extensive methylation of the mitochondrial genome appeared to be a ubiquitous, consistent feature of these cells and was present in both the high and low quality sperm populations. By contrast, the methylation status of the nuclear genome appeared to change dramatically in relation to the functional competence of the spermatozoa, such that defective cells exhibited a statistically significant increase in nuclear DNA methylation. Such hypermethylation of defective cells was confirmed by all 3 of the techniques used in this study (HPLC, immunocytochemistry and flow cytometry). Different patterns of 5-methylcytosine expression were observed sperm nuclei by immunocytochemistry and possible interpretations offered in terms of the packaging of chromosomes into the nucleus during sperm differentiation. Furthermore, the methylation status of these cells was negatively correlated with various aspects of sperm function including sperm motility and the tendency of these cells to become apoptotic as reflected by the expression of activated caspases and Annexin-V binding. In addition the hypermethylation of human spermatozoa was highly correlated with their capacity to bind chromomycin3A, a marker that reflects the efficiency of sperm chromatin protamination. These results clearly suggest that defective human spermatozoa are associated with hypermethylation of their nuclear genome, possibly as a consequence of the defective control of DNA methyltransferase activity during spermiogenesis. These hypermethylated cells are functionally defective and exhibit a tendency to default to an apoptotic cascade that features activation of endogenous caspases, phosphatidylserine exteriorization and DNA damage. These results have important implications for the safety of assisted conception procedures that frequently involve the forced fertilization of oocytes with defective spermatozoa

Advisors/Committee Members: University of Newcastle. Faculty of Health, School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: DNA; methylation; human sperm

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

APA (6^th Edition):

Barzideh, J. (2010). Epigenetic modification in human male germ line. (Masters Thesis). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/923302

Chicago Manual of Style (16^th Edition):

Barzideh, Jaleh. “Epigenetic modification in human male germ line.” 2010. Masters Thesis, University of Newcastle. Accessed February 19, 2020. http://hdl.handle.net/1959.13/923302.

MLA Handbook (7^th Edition):

Barzideh, Jaleh. “Epigenetic modification in human male germ line.” 2010. Web. 19 Feb 2020.

Vancouver:

Barzideh J. Epigenetic modification in human male germ line. [Internet] [Masters thesis]. University of Newcastle; 2010. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1959.13/923302.

Council of Science Editors:

Barzideh J. Epigenetic modification in human male germ line. [Masters Thesis]. University of Newcastle; 2010. Available from: http://hdl.handle.net/1959.13/923302

University of Southern California

16. Hinoue, Toshinori. DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications.

Degree: PhD, Biochemistry & Molecular Biology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/238424/rec/2063

► Aberrant DNA hypermethylation of CpG islands is a common and early event in colorectal tumorigenesis. Promoter DNA hypermethylation is associated with transcriptional gene silencing, and… (more)

▼ Aberrant DNA hypermethylation of CpG islands is a common and early event in colorectal tumorigenesis. Promoter DNA hypermethylation is associated with transcriptional gene silencing, and can contribute to tumorigenesis when it occurs at a critical tumor suppressor gene. A distinct subset of colorectal cancers display the CpG island methylator phenotype (CIMP), characterized by an exceptionally high frequency of cancer-specific DNA hypermethylation. Recent studies have shown that an activating mutation of BRAF (BRAFV600E) is specifically associated with CIMP. We used colorectal cancer cell lines and primary tumors to elucidate the molecular mechanisms for the association. We first examined whether expression of BRAFV600E causes CIMP-specific DNA hypermethylation in the CIMP-negative, BRAF wild-type COLO 320DM colorectal cancer cell line. We found that stable expression of BRAFV600E is not sufficient to induce CIMP in our system. Secondly, considering the alternative possibility, we searched for genes whose DNA hypermethylation was tightly linked to BRAFV600E and CIMP in colorectal cancer. Intriguingly, we identified CIMP-dependent DNA hypermethylation and transcriptional inactivation of IGFBP7, a mediator of BRAFV600E-induced cellular senescence and apoptosis. Inactivation of IGFBP7 by DNA hypermethylation may accommodate BRAFV600E by blocking the senescence pathway. Therefore, our work provides a mechanistic rationale for the association between BRAFV600E and CIMP. Moreover, in an attempt to further characterize CIMP-associated DNA hypermethylation, we have quantitatively determined DNA methylation status of 27,578 CpG sites located in 14,495 gene promoters in 100 colorectal tumors and 8 normal mucosae. Through stringent statistical methods, we have identified cancer-specific DNA hypermethylation of 1,036 genes, of which 601 show CIMP-specific DNA hypermethylation. We have also generated gene expression data.; Our most comprehensive list of CIMP targets and their expression data will help us understand the role of CIMP-associated DNA hypermethylation in colorectal tumorigenesis, and provide the opportunity to study structural and sequence characteristics of affected CpG islands. The latter might ultimately give us insights into the underlying basis of CIMP-associated DNA hypermethylation. Finally, we have developed a panel of novel cancer-specific DNA methylation markers, which would potentially be useful for early diagnosis of colorectal cancer using a noninvasive stool DNA test or a minimally invasive blood-based assay. Advisors/Committee Members: Laird, Peter W. (Committee Chair), Coetzee, Gerhard A. (Committee Member), Dubeau, Louis (Committee Member), Rice, Judd C. (Committee Member).

Subjects/Keywords: colorectal cancer; DNA methylation; CIMP

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APA (6^th Edition):

Hinoue, T. (2011). DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/238424/rec/2063

Chicago Manual of Style (16^th Edition):

Hinoue, Toshinori. “DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications.” 2011. Doctoral Dissertation, University of Southern California. Accessed February 19, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/238424/rec/2063.

MLA Handbook (7^th Edition):

Hinoue, Toshinori. “DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications.” 2011. Web. 19 Feb 2020.

Vancouver:

Hinoue T. DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications. [Internet] [Doctoral dissertation]. University of Southern California; 2011. [cited 2020 Feb 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/238424/rec/2063.

Council of Science Editors:

Hinoue T. DNA hypermethylation: its role in colorectal tumorigenesis and potential clinical applications. [Doctoral Dissertation]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/238424/rec/2063

17. Choi, Chang-Sui. Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/4135

Subjects/Keywords: DNA methylation

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

APA (6^th Edition):

Choi, C. (n.d.). Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/4135

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Choi, Chang-Sui. “Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed February 19, 2020. http://hdl.handle.net/10061/4135.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Choi, Chang-Sui. “Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ.” Web. 19 Feb 2020.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Choi C. Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10061/4135.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Choi C. Change of DNA methylation status in response to environmental stress : 環境に応答したDNAメチル化の変化; カンキョウニオウトウシタ DNA メチルカノヘンカ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/4135

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

18. Wada, Yuko. Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/2817

Subjects/Keywords: DNA methylation

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APA (6^th Edition):

Wada, Y. (n.d.). Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/2817

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wada, Yuko. “Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed February 19, 2020. http://hdl.handle.net/10061/2817.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wada, Yuko. “Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ.” Web. 19 Feb 2020.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Wada Y. Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10061/2817.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Wada Y. Biochemical properties and physiological function of DNA methyltransferases from tobacco plants : タバコDNAメチル化酵素の生化学的特徴と生理機能; タバコ DNA メチルカコウソノセイカガクテキトクチョウトセイリキノウ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/2817

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Penn State University

19. Abu Bakar, Nur Suhada. Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize.

Degree: MS, Agronomy, 2013, Penn State University

URL: https://etda.libraries.psu.edu/catalog/18226

► Epigenetics is the study of heritable changes in gene expression or cellular phenotype that are attributable to mechanisms other than changes in DNA sequence. In… (more)

▼ Epigenetics is the study of heritable changes in gene expression or cellular phenotype that are attributable to mechanisms other than changes in DNA sequence. In plants, epigenetic regulation plays a key role in various biological processes such as paramutation, genomic imprinting, and gene silencing. Although numerous studies have been done to elucidate the underlying mechanism behind epigenetic regulation, many questions are yet to be answered. In this study, the maize pericarp color1 (p1) gene is used as a reporter to study the nature of epigenetic inheritance of stable tissue-specific gene expression. An allele of p1, P1-wr was used as a phenotypic marker to investigate the transgenerational inheritance of Unstable factor for orange1 (Ufo1-1)-induced changes in maize. Ufo1-1 activates p1 expression and thus phlobaphenes are ectopically accumulated throughout the plant body indicating loss of tissue-specificity of p1 expression. Previous study has shown that Ufo1-1-induced pigmentation phenotypes are only observed in a subset of P1-wr; Ufo1-1 plants. Interestingly, within this subset, pigmentation level is highly variable. Also, it has been shown that this increased pigmentation is associated with changes of DNA methylation pattern in the P1-wr distal enhancer and intron sequences. Moreover, the increased pigmentation phenotypes in the backcross population are accompanied by progressive loss of P1-wr methylation from one generation to the next. Thus, the objective of this study was to investigate the inheritance of Ufo1-1 through genotyping using linked markers. This information was then compared to the Ufo1-1-induced phenotypes to verify the epigenetic regulation of P1-wr by Ufo1-1. The second objective of this study was to establish a qRT-PCR based assay to investigate DNA methylation level at p1 in different genotypes of P1-wr; Ufo1-1 plants. The relative methylation levels provided better understanding of the correlation between the range of pericarp pigmentation in P1-wr; Ufo1-1 plants and their respective DNA methylation states at p1.

Subjects/Keywords: epigenetics; DNA methylation; inheritance

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APA (6^th Edition):

Abu Bakar, N. S. (2013). Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize. (Masters Thesis). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/18226

Chicago Manual of Style (16^th Edition):

Abu Bakar, Nur Suhada. “Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize.” 2013. Masters Thesis, Penn State University. Accessed February 19, 2020. https://etda.libraries.psu.edu/catalog/18226.

MLA Handbook (7^th Edition):

Abu Bakar, Nur Suhada. “Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize.” 2013. Web. 19 Feb 2020.

Vancouver:

Abu Bakar NS. Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize. [Internet] [Masters thesis]. Penn State University; 2013. [cited 2020 Feb 19]. Available from: https://etda.libraries.psu.edu/catalog/18226.

Council of Science Editors:

Abu Bakar NS. Transgenerational inheritance of epigenetic regulation by Unstable factor for orange1 in maize. [Masters Thesis]. Penn State University; 2013. Available from: https://etda.libraries.psu.edu/catalog/18226

University of Edinburgh

20. Playfoot, Christopher James. Genome defence in hypomethylated developmental contexts.

Degree: PhD, 2017, University of Edinburgh

URL: http://hdl.handle.net/1842/28783

► Retrotransposons constitute around 40% of the mammalian genome and their aberrant activation can have wide ranging detrimental consequences, both throughout development and into somatic lineages.… (more)

▼ Retrotransposons constitute around 40% of the mammalian genome and their aberrant activation can have wide ranging detrimental consequences, both throughout development and into somatic lineages. DNA methylation is one of the major epigenetic mechanisms in mammals, and is essential in repressing retrotransposons throughout mammalian development. Yet during normal mouse embryonic development some cell lineages become extensively DNA hypomethylated and it is not clear how these cells maintain retrotransposon silencing in a globally hypomethylated genomic context. In this thesis I determine that hypomethylation in multiple contexts results in the consistent activation of only one gene in the mouse genome - Tex19.1. Thus if a generic compensatory mechanism for loss of DNA methylation exists in mice, it must function through this gene. Tex19.1-/- mice de-repress retrotransposons in the hypomethylated component of the placenta and in the mouse germline, and have developmental defects in these tissues. In this thesis I examine the mechanism of TEX19.1 mediated genome defence and the developmental consequences upon its removal. I show that TEX19.1 functions in repressing retrotransposons, at least in part, through physically interacting with the transcriptional co-repressor, KAP1. Tex19.1-/- ES cells have reduced levels of KAP1 bound retrotransposon chromatin and reduced levels of the repressive H3K9me3 modification at these loci. Furthermore, these subsets of retrotransposon loci are de-repressed in Tex19.1-/- placentas. Thus, my data indicates that mouse cells respond to hypomethylation by activating expression of Tex19.1, which in turn augments compensatory, repressive histone modifications at retrotransposon sequences, thereby helping developmentally hypomethylated cells to maintain genome stability. I next aimed to further elucidate the role of Tex19.1 in the developing hypomethylated placenta. I determine that Tex19.1-/- placental defects precede intrauterine growth restriction of the embryo and that alterations in mRNA abundance in E12.5 Tex19.1-/- placentas is likely in part due to genic transcriptional changes. De-repression of LINE- 1 is evident in these placentas and elements of the de-repressed subfamily are associated with significantly downregulated genes. If retrotransposon de-repression is contributing to developmental defects by interfering with gene expression remains to be determined, however I identify a further possible mechanism leading to placental developmental defects. I determine that Tex19.1-/- placentas have an increased innate immune response and I propose that this is contributing to the developmental defects observed. Developmental defects and retrotransposon de-repression are also observed in spermatogenesis in Tex19.1-/- testes, the molecular basis for which is unclear. I therefore investigate the possibility that the TEX19.1 interacting partners, the E3 ubiquitin ligase proteins, may be contributing to the phenotypes observed in Tex19.1- /- testes. I show that repression of MMERVK10C in the…

Subjects/Keywords: DNA methylation; Tex19.1; retrotransposons

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APA (6^th Edition):

Playfoot, C. J. (2017). Genome defence in hypomethylated developmental contexts. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/28783

Chicago Manual of Style (16^th Edition):

Playfoot, Christopher James. “Genome defence in hypomethylated developmental contexts.” 2017. Doctoral Dissertation, University of Edinburgh. Accessed February 19, 2020. http://hdl.handle.net/1842/28783.

MLA Handbook (7^th Edition):

Playfoot, Christopher James. “Genome defence in hypomethylated developmental contexts.” 2017. Web. 19 Feb 2020.

Vancouver:

Playfoot CJ. Genome defence in hypomethylated developmental contexts. [Internet] [Doctoral dissertation]. University of Edinburgh; 2017. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1842/28783.

Council of Science Editors:

Playfoot CJ. Genome defence in hypomethylated developmental contexts. [Doctoral Dissertation]. University of Edinburgh; 2017. Available from: http://hdl.handle.net/1842/28783

Oregon State University

21. Vargason, Jeffrey M. The effect of cytosine methylation on DNA structure.

Degree: PhD, Biochemistry and Biophysics, 2002, Oregon State University

URL: http://hdl.handle.net/1957/32388

► DNA methylation is common in prokaryotes and eukaryotes and has been implicated in various biological roles including gene silencing, X-chromosome inactivation, and genomic imprinting. 5-methylcytosine… (more)

▼ DNA methylation is common in prokaryotes and eukaryotes and has been implicated in various biological roles including gene silencing, X-chromosome inactivation, and genomic imprinting. 5-methylcytosine the "fifth base" of the genetic code comprises 1-3% of the human genome and is primarily found on cytosines within the context of the CpG sequence. Although progress has been made in understanding the biological roles of 5-methylcytosine, we are only beginning to uncover how it changes the local structure and global conformation of DNA. This thesis deals with the local perturbations in structure and hydration and the global conformational changes induced by the presence of 5-methylcytosine in DNA as determined by single crystal x-ray diffraction. 5-methylcytosine induces a novel conformation in the structure of duplex DNA. This conformation has characteristics of both the A-DNA and B-DNA conformations as well as some unique defining characteristics. This distinct duplex provides a structural rationale for the increased rate of deamination in 5-methylcytosine relative to cytosine. In addition to this novel conformation, 5-methylcytosine stabilizes intermediates within the B-DNA to A-DNA transition pathway, thus providing a crystallographic map of the transition from B-DNA to A-DNA. 5-methylcytosine was also used as a tool to probe the stabilizing features of the DNA four-way junction (known as the Holliday junction). The first crystal structures of Holliday junctions were found serendipitously while studying duplex DNA. The DNA four-way junction formation in these crystals was thought to be stabilized by a network of sequence dependent hydrogen bonds at the junction crossover. In this thesis, 5-methylcytosine was used to perturb these hydrogen bonds; however, the junction persisted, suggesting that there is flexibility in the types of sequences that can accommodate junction formation in the crystal, as well as, flexibility in the global structure of the junction. Overall, this work describes the effects of 5-methylcytosine on the local and global structure and hydration of DNA structure, as well as raising some interesting questions regarding the biological impact of methylation induced DNA structure. Advisors/Committee Members: Ho, Pui Shing (advisor).

Subjects/Keywords: DNA – Methylation

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

APA (6^th Edition):

Vargason, J. M. (2002). The effect of cytosine methylation on DNA structure. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/32388

Chicago Manual of Style (16^th Edition):

Vargason, Jeffrey M. “The effect of cytosine methylation on DNA structure.” 2002. Doctoral Dissertation, Oregon State University. Accessed February 19, 2020. http://hdl.handle.net/1957/32388.

MLA Handbook (7^th Edition):

Vargason, Jeffrey M. “The effect of cytosine methylation on DNA structure.” 2002. Web. 19 Feb 2020.

Vancouver:

Vargason JM. The effect of cytosine methylation on DNA structure. [Internet] [Doctoral dissertation]. Oregon State University; 2002. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1957/32388.

Council of Science Editors:

Vargason JM. The effect of cytosine methylation on DNA structure. [Doctoral Dissertation]. Oregon State University; 2002. Available from: http://hdl.handle.net/1957/32388

Oregon State University

22. Bononi, Judy. Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies.

Degree: MS, Biochemistry and Biophysics, 1994, Oregon State University

URL: http://hdl.handle.net/1957/35264

Subjects/Keywords: DNA – Methylation

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APA (6^th Edition):

Bononi, J. (1994). Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/35264

Chicago Manual of Style (16^th Edition):

Bononi, Judy. “Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies.” 1994. Masters Thesis, Oregon State University. Accessed February 19, 2020. http://hdl.handle.net/1957/35264.

MLA Handbook (7^th Edition):

Bononi, Judy. “Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies.” 1994. Web. 19 Feb 2020.

Vancouver:

Bononi J. Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies. [Internet] [Masters thesis]. Oregon State University; 1994. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1957/35264.

Council of Science Editors:

Bononi J. Effect of hemi-methylated CG dinucleotide on Z-DNA stability : crystallographic and solution studies. [Masters Thesis]. Oregon State University; 1994. Available from: http://hdl.handle.net/1957/35264

23. Gentil, Marie-Véronique. Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool.

Degree: Docteur es, Physiologie et biologie des organismes et des populations, 2009, Université d'Orléans

URL: http://www.theses.fr/2009ORLE2005

►

Chez les plantes, les processus de développement global et de plasticité développementale sont contrôlés par des mécanismes épigénétiques. La méthylation de l’ADN peut présenter un… (more)

▼

Chez les plantes, les processus de développement global et de plasticité développementale sont contrôlés par des mécanismes épigénétiques. La méthylation de l’ADN peut présenter un polymorphisme (épiallèles) qui est une source possible de biomarqueurs pour la sélection de génotypes d’intérêt agronomique. Pourtant, la recherche de tels biomarqueurs n’a pas encore été initiée. Dans ce contexte, nos objectifs ont concerné l'élaboration d'une stratégie pour la mise en évidence d’un contrôle épigénétique lors d’un processus développemental chez la betterave sucrière (Beta vulgaris altissima), ainsi que la recherche des biomarqueurs épigénétiques associés. Cette stratégie a d’abord été appliquée à la morphogenèse in vitro, sur trois lignées cellulaires de betterave sucrière. Une relation a pu être établie entre le niveau de méthylation de l’ADN et les propriétés morphogénétiques des lignées. Des biomarqueurs de morphogenèse in vitro ont ainsi été identifiés. La même stratégie a ensuite été appliquée in planta à la même espèce. L'existence d'un contrôle épigénétique lors de la vernalisation et de la dévernalisation chez plusieurs hybrides de betterave sucrière, avec des sensibilités à la montaison différentes, a été démontrée. Nous suggérons que l’amplitude et la cinétique des variations épigénétiques contrôlent l’induction de la montaison et sa rapidité, confirmant ainsi le rôle de la méthylation de l’ADN dans ce processus. Les loci cibles de ces remaniements de la méthylation de l'ADN lors de la vernalisation ont été définis. Un criblage a enfin permis d’identifier de potentiels biomarqueurs épigénétiques de la sensibilité à la montaison en vue de la mise au point d’un futur test de sélection agronomique.

In plants, the processes of global development and of developmental plasticity are controlled by epigenetic mechanisms. Polymorphism in DNA methylation (leading to epialleles) is a possible source of biomarkers for the selection of genotypes of agronomic interest. Until now, however, the search for such biomarkers has not been undertaken. Against this background, our objectives were to develop a strategy to investigate the existence of epigenetic control during a developmental process in sugar-beet (Beta vulgaris altissima) and to search for associated epigenetic biomarkers. The strategy was first applied to three sugar-beet cell lines, where we were able to established a relationship between the level of DNA methylation and the morphogenetic statue of the lines, and thus to identified a number of biomarkers for in vitro morphogenesis. We then applied the same strategy in planta in the same species and demonstrated the existence of epigenetic control (DNA methylation) during vernalization and devernalization in several sugar-beet hybrids that differed for bolting susceptibility. We propose that the scale and kinetics of epigenetic modifications control the induction and the rapidity of bolting, confirming the role of DNA methylation in this process. We have identified a number of target loci for these changes in DNA…

Advisors/Committee Members: Hagège, Daniel (thesis director), Maury, Stéphane (thesis director).

Subjects/Keywords: Méthylation de l'ADN; DNA methylation

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

APA (6^th Edition):

Gentil, M. (2009). Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool. (Doctoral Dissertation). Université d'Orléans. Retrieved from http://www.theses.fr/2009ORLE2005

Chicago Manual of Style (16^th Edition):

Gentil, Marie-Véronique. “Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool.” 2009. Doctoral Dissertation, Université d'Orléans. Accessed February 19, 2020. http://www.theses.fr/2009ORLE2005.

MLA Handbook (7^th Edition):

Gentil, Marie-Véronique. “Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool.” 2009. Web. 19 Feb 2020.

Vancouver:

Gentil M. Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool. [Internet] [Doctoral dissertation]. Université d'Orléans; 2009. [cited 2020 Feb 19]. Available from: http://www.theses.fr/2009ORLE2005.

Council of Science Editors:

Gentil M. Contrôle épigénétique du risque de montaison chez une plante de grande culture : la betterave sucrière : mise au point d'une stratégie de caractérisation d'épiallèles associés à la sensibilité à la montaison en vue de l'élaboration d'un test de sélection : Epigenetic control of the bolting risk in a crop plant : sugar-beet : the development of a strategy to characterize epialleles associated with bolting sensivity, with a view to implementation as a selection tool. [Doctoral Dissertation]. Université d'Orléans; 2009. Available from: http://www.theses.fr/2009ORLE2005

Columbia University

24. Wang, Ya. Statistical Methods for Epigenetic Data.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-9z87-ts07

► DNA methylation plays a crucial role in human health, especially cancer. Traditional DNA methylation analysis aims to identify CpGs/genes with differential methylation (DM) between experimental… (more)

▼ DNA methylation plays a crucial role in human health, especially cancer. Traditional DNA methylation analysis aims to identify CpGs/genes with differential methylation (DM) between experimental groups. Differential variability (DV) was recently observed that contributes to cancer heterogeneity and was also shown to be essential in detecting early DNA methylation alterations, notably epigenetic field defects. Moreover, studies have demonstrated that environmental factors may modify the effect of DNA methylation on health outcomes, or vice versa. Therefore, this dissertation seeks to develop new statistical methods for epigenetic data focusing on DV and interactions when efficient analytical tools are lacking. First, as neighboring CpG sites are usually highly correlated, we introduced a new method to detect differentially methylated regions (DMRs) that uses combined DM and DV signals between diseased and non-diseased groups. Next, using both DM and DV signals, we considered the problem of identifying epigenetic field defects, when CpG-site-level DM and DV signals are minimal and hard to be detected by existing methods. We proposed a weighted epigenetic distance-based method that accumulates CpG-site-level DM and DV signals in a gene. Here DV signals were captured by a pseudo-data matrix constructed using centered quadratic methylation measures. CpG-site-level association signal annotations were introduced as weights in distance calculations to up-weight signal CpGs and down-weight noise CpGs to further boost the study power. Lastly, we extended the weighted epigenetic distance-based method to incorporate DNA methylation by environment interactions in the detection of overall association between DNA methylation and health outcomes. A pseudo-data matrix was constructed with cross-product terms between DNA methylation and environmental factors that is able to capture their interactions. The superior performance of the proposed methods were shown through intensive simulation studies and real data applications to multiple DNA methylation data.

Subjects/Keywords: Biometry; Epigenetics; DNA – Methylation; Statistics

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APA (6^th Edition):

Wang, Y. (2019). Statistical Methods for Epigenetic Data. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-9z87-ts07

Chicago Manual of Style (16^th Edition):

Wang, Ya. “Statistical Methods for Epigenetic Data.” 2019. Doctoral Dissertation, Columbia University. Accessed February 19, 2020. https://doi.org/10.7916/d8-9z87-ts07.

MLA Handbook (7^th Edition):

Wang, Ya. “Statistical Methods for Epigenetic Data.” 2019. Web. 19 Feb 2020.

Vancouver:

Wang Y. Statistical Methods for Epigenetic Data. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2020 Feb 19]. Available from: https://doi.org/10.7916/d8-9z87-ts07.

Council of Science Editors:

Wang Y. Statistical Methods for Epigenetic Data. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-9z87-ts07

University of Melbourne

25. NOVAKOVIC, BORIS. Epigenetics of human placental development and pregnancy-associated disease.

Degree: 2013, University of Melbourne

URL: http://hdl.handle.net/11343/38191

► INTRODUCTION: Epigenetics literally means ‘above DNA’ and refers to the study of molecular modifications that control gene expression and chromatin structure. DNA methylation, the most… (more)

▼ INTRODUCTION: Epigenetics literally means ‘above DNA’ and refers to the study of molecular modifications that control gene expression and chromatin structure. DNA methylation, the most extensively studied epigenetic modification, is involved in both the maintenance of chromosome stability and gene expression. Due to its role in gene expression, tissue specific DNA methylation patterns are assumed to reflect the function of a specific gene in a particular tissue. The human placenta facilitates the interaction between the mother and the fetus, including nutrient and oxygen exchange, waste removal and the protection of the fetus from the maternal immune response. Due to its role at the feto-maternal interface, the placenta is exposed to several environmental factors with the capacity to alter placental function and fetal development. Many of these effects are likely to be mediated by epigenetic change. Linking specific environmental exposures, genetic, and epigenetic variation to maternal and neonatal outcomes may provide valuable mechanistic insights into the role of placental dysfunction in pregnancy-associated disease and later health. Therefore, DNA methylation studies in healthy and disease placentas have the potential to identify new genes associated with placental function. The aim of this PhD was to take a genome-scale approach to characterise gene promoter methylation in the normal human placenta. MATERIALS AND METHODS: Several different tissues, primary cells and cell lines were used in this study. These included placental villi from first, second and third trimester, purified first trimester villous and extravillous cytotrophoblasts, choriocarcinoma and trophoblast-derived cell lines. Placental tissue, neonatal cord blood and maternal peripheral blood serum from twin births, collected as part of the Peri/post-natal Epigenetic Twins Study (PETS) cohort, were used for two aims of this project. Environmental data on maternal nutrition and supplementation during pregnancy were collected through questionnaires or measured in maternal blood serum. DNA methylation levels were analysed on the genome-scale level using the Illumina Infinium HumanMethylation27 BeadChip, and at the gene-specific level using the SEQUENOM MassARRAY EpiTYPER platform. RESULTS: Genome-scale DNA methylation analysis of normal human placenta from first to third trimester identified dynamic changes in DNA methylation patterns in response to increasing gestation and environmental/stochastic factors. Most of the changes were observed at genes involved in immune cell communication and signalling, which likely reflects the change in cell composition as well as the differing immunological interactions between the mother and the fetus as the pregnancy progresses. Furthermore, increasing inter-individual variation in methylation level at certain CpG sites over gestation…

Subjects/Keywords: epigenetics; DNA methylation; placenta; environment

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

APA (6^th Edition):

NOVAKOVIC, B. (2013). Epigenetics of human placental development and pregnancy-associated disease. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38191

Chicago Manual of Style (16^th Edition):

NOVAKOVIC, BORIS. “Epigenetics of human placental development and pregnancy-associated disease.” 2013. Doctoral Dissertation, University of Melbourne. Accessed February 19, 2020. http://hdl.handle.net/11343/38191.

MLA Handbook (7^th Edition):

NOVAKOVIC, BORIS. “Epigenetics of human placental development and pregnancy-associated disease.” 2013. Web. 19 Feb 2020.

Vancouver:

NOVAKOVIC B. Epigenetics of human placental development and pregnancy-associated disease. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/11343/38191.

Council of Science Editors:

NOVAKOVIC B. Epigenetics of human placental development and pregnancy-associated disease. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38191

University of Edinburgh

26. Perricone, Sara Maria. The role of DNA methylation in transcriptional regulation.

Degree: PhD, 2015, University of Edinburgh

URL: http://hdl.handle.net/1842/17866

► In mammals, the correct spatio-temporal patterns of gene expression are coordinated by transcription factor networks in combination with epigenetic signalling pathways. CpG methylation is an… (more)

▼ In mammals, the correct spatio-temporal patterns of gene expression are coordinated by transcription factor networks in combination with epigenetic signalling pathways. CpG methylation is an epigenetic modification of DNA involved in the heritable transmission of gene silencing patterns. Increasing evidence suggest a primary role for CpG methylation in the direct regulation of gene expression, at least for a subset of promoters. An example of this direct regulation is represented by the ectopic expression of genes involved in genome defence pathways upon global loss of methylation. However, the mechanistic relationship between CpG methylation and transcriptional regulation is not well understood. To explore this, we have applied Cap Analysis of Gene Expression (CAGE), to cells deficient in CpG methylation (Mouse Embryonic Fibroblasts with hypomorphic mutation of Dnmt1 ) and matched controls. This provides a quantitative, single nucleotide resolution, genome wide map of methylation responsive transcription initiation. Integrating this with RNA-seq, genome wide measures of CpG methylation and ChIP-seq for histone modifications in the same system, provides a detailed view of how reduced CpG methylation alters the chromatin and transcriptional landscape of the genome. Our results show dramatic shifts in the cellular RNA pool, with the pronounced up-regulation or de-repression of promoters in a specific sub-family of transposable elements. Tens of other genic and non-coding RNA promoters similarly show dramatic inductions. Contrary to a prior hypothesis, we found no evidence for increased rates of transcriptional initiation from anonymous genomic sites not previously implicated in promoter activity. Transcription initiation at CpG island promoters is generally unaffected by hypomethylation, however a set of TSSs located in CpG island shores and a class to transposable element overlapping TSSs do appear to be sensitive to methylation and are significantly up-regulated upon hypomethylation.

Subjects/Keywords: 572.8; DNA methylation; transcription; hypomethylation

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

APA (6^th Edition):

Perricone, S. M. (2015). The role of DNA methylation in transcriptional regulation. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/17866

Chicago Manual of Style (16^th Edition):

Perricone, Sara Maria. “The role of DNA methylation in transcriptional regulation.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed February 19, 2020. http://hdl.handle.net/1842/17866.

MLA Handbook (7^th Edition):

Perricone, Sara Maria. “The role of DNA methylation in transcriptional regulation.” 2015. Web. 19 Feb 2020.

Vancouver:

Perricone SM. The role of DNA methylation in transcriptional regulation. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1842/17866.

Council of Science Editors:

Perricone SM. The role of DNA methylation in transcriptional regulation. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/17866

University of North Carolina – Greensboro

27. Rumph, Candie. Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells.

Degree: 2014, University of North Carolina – Greensboro

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16604

► WNT5A is a secreted ligand involved in differentiation, proliferation, cell movement and apoptosis. WNT5A is often misregulated in cancer and is known to be involved… (more)

▼ WNT5A is a secreted ligand involved in differentiation, proliferation, cell movement and apoptosis. WNT5A is often misregulated in cancer and is known to be involved in cancer metastasis. The focus of this study was on the possible epigenetic regulation of WNT5A expression in osteosarcoma cells. In this study, I analyzed WNT5A regulation from its two major transcription start sites, termed Promoter A and Promoter B. The levels of promoter B transcripts were reduced in the osteosarcoma cell line, U20S, and in primary osteosarcoma tissue of three individuals, compared to normal osteoblasts. To determine if this decrease in Promoter B activity in U20S is due to DNA methylation, I analyzed six CpG islands associated with Promoter B by bisulfite sequencing. Results show that Regions 1 and 2 are unmethylated, Regions 3, 4, 5 are methylated and Region 6, which includes the Promoter B start of transcription, is partially methylated. The DNA methylation pattern is similar to the pattern determined in another osteosarcoma cell line SaOS-2. However, Region 6 of U20S is only 25% methylated, whereas Region 6 of SaOS-2 is 62% methylated. The level of methylation is negatively correlated with Promoter B transcript levels, indicating that Region 6 methylation affects transcription. Histone modifications were examined for their involvement in Promoter A and Promoter B activity by chromatin immunoprecipitation (ChIP) assays. H3K4me3, an activating histone mark, showed high enrichment in Promoter A and reduced enrichment in Promoter B Region 6 of U20S cells, indicating that H3K4me3 has a role in the reduction of Promoter B activity. H3K27me3 and H3K9me3, repressive histone marks, were not differentially enriched on Promoters A and B. H3K27me3 was enriched on Regions 3 and 4 located upstream of the Promoter B start of transcription. Overall, these results suggest that WNT5A Promoter B activity is reduced in osteosarcoma by both histone modification and DNA methylation.; WNT5A, Osteosarcoma Cells, DNA methylation Advisors/Committee Members: Karen Katula (advisor).

Subjects/Keywords: Wnt proteins; DNA – Methylation; Osteosarcoma

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APA (6^th Edition):

Rumph, C. (2014). Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells. (Masters Thesis). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16604

Chicago Manual of Style (16^th Edition):

Rumph, Candie. “Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells.” 2014. Masters Thesis, University of North Carolina – Greensboro. Accessed February 19, 2020. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16604.

MLA Handbook (7^th Edition):

Rumph, Candie. “Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells.” 2014. Web. 19 Feb 2020.

Vancouver:

Rumph C. Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells. [Internet] [Masters thesis]. University of North Carolina – Greensboro; 2014. [cited 2020 Feb 19]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16604.

Council of Science Editors:

Rumph C. Aberrant DNA methylation and patterns of histone modifications at the WNT5A Promoter B in osteosarcoma cells. [Masters Thesis]. University of North Carolina – Greensboro; 2014. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16604

University of Edinburgh

28. Moffat, Michael. Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes.

Degree: PhD, 2016, University of Edinburgh

URL: http://hdl.handle.net/1842/25711

► Transcriptional repression is maintained by many molecular processes, including DNA methylation and polycomb repression. These two systems are both associated with chromatin modification at the… (more)

Subjects/Keywords: DNA methylation; chromatin; epigenetics; polycomb

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

APA (6^th Edition):

Moffat, M. (2016). Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/25711

Chicago Manual of Style (16^th Edition):

Moffat, Michael. “Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes.” 2016. Doctoral Dissertation, University of Edinburgh. Accessed February 19, 2020. http://hdl.handle.net/1842/25711.

MLA Handbook (7^th Edition):

Moffat, Michael. “Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes.” 2016. Web. 19 Feb 2020.

Vancouver:

Moffat M. Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes. [Internet] [Doctoral dissertation]. University of Edinburgh; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1842/25711.

Council of Science Editors:

Moffat M. Aberrant DNA modification profiles in embryonic stem cells lacking polycomb repressive complexes. [Doctoral Dissertation]. University of Edinburgh; 2016. Available from: http://hdl.handle.net/1842/25711

29. Pollak, Adam Jacob. Rethinking How Proteins Move Along DNA.

Degree: 2014, University of California – eScholarship, University of California

URL: http://www.escholarship.org/uc/item/1nc2s6fx

► Site-specific DNA binding by proteins is critical for diverse biological processes, including gene regulation, DNA repair, DNA replication, immune response, and others. In most cases,… (more)

▼ Site-specific DNA binding by proteins is critical for diverse biological processes, including gene regulation, DNA repair, DNA replication, immune response, and others. In most cases, this binding is preceded by facilitated diffusion, where the protein passively moves along nonspecific DNA (DNA lacking particular binding sites) in search of its site(s). Details concerning the mechanisms of how proteins move along DNA remain unclear yet actively investigated. Several reports claim that facilitated diffusion relies primarily on sliding and hopping processes, where the protein moves along the trajectory of the DNA helix. However, these mechanisms involve redundant searches over local regions (up to hundreds of base pairs), while site finding in vivo requires searches of hundreds of thousands of base pairs. We "rethink" facilitated diffusion in two ways: 1) what are the mechanisms available for facilitated diffusion? And 2) how are these mechanisms driven by proteins' specific biological context? We investigate the facilitated diffusion properties of E. coli DNA adenine methyltransferase (Dam), which methylates palindromic 5'-GATC-3' sites on the N6 position of adenine. We use an in vitro steady-state processivity assay, where the ability of the enzyme to catalyze multiple methylations within a single binding event is quantified. Our results are suggestive of a new mechanism, intersegmental hopping, where proteins hop between regions of a single DNA molecule that are looped together. This mechanism allows for efficient long-range movements, and is similar to other ambiguously described looping mechanisms proposed in recent reports. Dam's low cellular copy number and need to move along the entire bacterial chromosome (i.e. its biological context) is ideally accommodated by this mechanism, as we imagine will be true for other proteins with low copy numbers and rare sites. We also demonstrate that EcoRI ENase uses an extreme sliding mechanism, previously hypothesized to be unlikely. EcoRI ENase and EcoRV ENase both cut incoming phage DNA as part of type II restriction modification systems, and are shown here to use distinct facilitated diffusion mechanisms. We argue that their site finding mechanisms are complimentary, ensuring robust phage defense, again demonstrating the connection between facilitated diffusion and biological context. Furthermore, we show that Dam is able to move along DNA in spite of pre-incubated protein roadblocks. Provocatively, DNA-loop inducing roadblocks, such as the histone-like Lrp, can improve the translocation process by specifically enhancing intersegmental hopping. Therefore, this mechanism is proposed as a general way for proteins to move along the crowded, compacted genomic DNA landscape. Dam was previously demonstrated to undergo intrasite processivity, where the methylation of both strands within a single GATC site proceeds by a single Dam enzyme dramatically reorienting itself while switching between strands. Here, we show that intrasite processivity is only possible on long stretches…

Subjects/Keywords: Chemistry; Biochemistry; DNA; Enzymes; Methylation

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

APA (6^th Edition):

Pollak, A. J. (2014). Rethinking How Proteins Move Along DNA. (Thesis). University of California – eScholarship, University of California. Retrieved from http://www.escholarship.org/uc/item/1nc2s6fx

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):

Pollak, Adam Jacob. “Rethinking How Proteins Move Along DNA.” 2014. Thesis, University of California – eScholarship, University of California. Accessed February 19, 2020. http://www.escholarship.org/uc/item/1nc2s6fx.

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

MLA Handbook (7^th Edition):

Pollak, Adam Jacob. “Rethinking How Proteins Move Along DNA.” 2014. Web. 19 Feb 2020.

Vancouver:

Pollak AJ. Rethinking How Proteins Move Along DNA. [Internet] [Thesis]. University of California – eScholarship, University of California; 2014. [cited 2020 Feb 19]. Available from: http://www.escholarship.org/uc/item/1nc2s6fx.

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

Council of Science Editors:

Pollak AJ. Rethinking How Proteins Move Along DNA. [Thesis]. University of California – eScholarship, University of California; 2014. Available from: http://www.escholarship.org/uc/item/1nc2s6fx

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

University of New South Wales

30. Yu, Albert. Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs.

Degree: Biotechnology & Biomolecular Sciences, 2016, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/56093 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:40011/SOURCE02?view=true

► LncRNAs are a class of nucleic acids that have been widely demonstrated to be involved in transcriptional regulation through epigenetic regulation via DNA methylation and… (more)

Subjects/Keywords: Nucleic acids; DNA methylation

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

APA (6^th Edition):

Yu, A. (2016). Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/56093 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:40011/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Yu, Albert. “Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs.” 2016. Masters Thesis, University of New South Wales. Accessed February 19, 2020. http://handle.unsw.edu.au/1959.4/56093 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:40011/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Yu, Albert. “Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs.” 2016. Web. 19 Feb 2020.

Vancouver:

Yu A. Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs. [Internet] [Masters thesis]. University of New South Wales; 2016. [cited 2020 Feb 19]. Available from: http://handle.unsw.edu.au/1959.4/56093 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:40011/SOURCE02?view=true.

Council of Science Editors:

Yu A. Integrative Genome-Wide Analysis of DNA Methyltransferase 3A Reveals a Novel Model of Transcriptional Regulation Modulated by Long Non-coding RNAs. [Masters Thesis]. University of New South Wales; 2016. Available from: http://handle.unsw.edu.au/1959.4/56093 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:40011/SOURCE02?view=true

Open Access Theses and Dissertations