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Academic literature on the topic 'DNA methylation'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 October 2024

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Journal articles on the topic "DNA methylation"

1

Mikaelsson, Mikael A., and Courtney A. Miller. "DNA methylation." Epigenetics 6, no. 5 (May 2011): 548–51. http://dx.doi.org/10.4161/epi.6.5.15679.

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Singal, Rakesh, and Gordon D. Ginder. "DNA Methylation." Blood 93, no. 12 (June 15, 1999): 4059–70. http://dx.doi.org/10.1182/blood.v93.12.4059.

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Singal, Rakesh, and Gordon D. Ginder. "DNA Methylation." Blood 93, no. 12 (June 15, 1999): 4059–70. http://dx.doi.org/10.1182/blood.v93.12.4059.412k40_4059_4070.

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Dang, Pengtao, Xiao Wang, Haiqi Zhu, Jia Wang, Tingbo Guo, Xinyu Zhou, Paveethran Swaminathan, Chi Zhang, and Sha Cao. "Abstract 5352: Targeting DNA methylation in T cells to improve the efficacy of immunotherapy." Cancer Research 83, no. 7_Supplement (April 4, 2023): 5352. http://dx.doi.org/10.1158/1538-7445.am2023-5352.

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Abstract T-cells are critical mediators of immunity and immunologic memory. Their cell fates are regulated in part through epigenetic mechanisms, including DNA methylation. Recent genome-wide methylation analyses have revealed dynamic alterations in the methylome at various stages of development and differentiation of T cells. At single cell level, it is not easy to simultaneously collect RNA-seq and RBBS methylation profiling. An important task is to understand the expression change of which genes and pathways are regulated by DNA methylations, especially for the ones that are associated with functional variations in the T cells from tumor microenvironment.In this study, we developed a computational approach based on our recently developed metabolic flux estimation to estimate cell-wise global DNA methylation activity level by using scRNA-seq data. We also hypothesize that the global DNA methylation activity level in one cell determines most of the DNA methylation level in gene-specific DNA methylations. Hence, the dependency between gene-specific DNA methylation and expression could be imputed by the dependency between predicted global DNA methylation input level and the gene expression. We validated our method to impute cell-wise global DNA methylation level by using four independent sets of paired gene expression and DNA methylation data. Noted, our prediction of global DNA methylation activity is from a pure metabolic perspective. We found that two metabolic reaction rates, named metabolic flux from methionine to SAM and SAM to SAH, purely predicted by using gene expression data can accurately impute DNA methylation activity in all validating data sets. Our method enables further identification of the disease/cell context specific contributor of DNA methylation, i.e., the genes high contribution to DNA methylations in each individual cell or cell groups. We applied our method on scRNA-seq data of different T cell types extracted from TME of lung, liver, and colon cancer. We have seen that exhausted T cells, especially the ones with decreased Granzymes and PRF1 are associated with increased global DNA methylation level and related genes, suggesting the potential clinical implications in targeting DNA methylation to improve the efficacy of immunotherapies. Citation Format: Pengtao Dang, Xiao Wang, Haiqi Zhu, Jia Wang, Tingbo Guo, Xinyu Zhou, Paveethran Swaminathan, Chi Zhang, Sha Cao. Targeting DNA methylation in T cells to improve the efficacy of immunotherapy. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5352.

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KARAASLAN, Ezgi, Ceren ACAR, and Şükrü KARTALCI. "Şizofrenide Epigenetik Bakış Açısı: DNA Metilasyon Modelleri." Arşiv Kaynak Tarama Dergisi 31, no. 3 (September 30, 2022): 204–12. http://dx.doi.org/10.17827/aktd.1096901.

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Schizophrenia is a mental disorder characterized by delusions, hallucinations and various behavioral disorders. Affecting approximately 1% of the world's population, schizophrenia not only affects patients, but also other members of the society. Genetic and environmental factors play roles in the etiology of the disorder.Genetics, neurodevelopmental disorder, drug use, urban life, alone or together can be counted as the factors that cause the disorder. Despite increasing studies in recent years, the factors causing the formation of schizophrenia have not been fully clarified and more research is needed. Although genetic factors are risk factors for schizophrenia, it is thought that some environmental factors affect the emergence of the disorder. Epigenetic mechanisms regulate gene functions without changing the nucleotide sequence of DNA. DNA methylation is associated with schizophrenia, and methylation status studies have been conducted in many schizophrenia candidate genes. Examination of DNA methylation states will contribute significantly to psychiatric research.In this review, data published in global databases obtained from DNA methylation studies related with schizophrenia are summarized and their importance in schizophrenia is briefly discussed.

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Sermswan, R., S. Mongkolsuk, and S. Sirisinha. "Characterization of the Opisthorchis viverrini genome." Journal of Helminthology 65, no. 1 (March 1991): 51–54. http://dx.doi.org/10.1017/s0022149x00010439.

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ABSTRACTThe methylations of trematode genomic DNA were analyzed using restriction enzymes and Southern blot hybridization. Restriction enzymes MspI, HpaII, HhaI were used to probe CpG methylation while MboI, Sau3A, DpnI were used for A methylation. The results revealed that Opisthorchis viverrini, Fasciola gigantica and Gigantocotyle siamensis had neither CpG nor A methylations. The presence of highly repeated DNA elements was also demonstrated in O. viverrini genomic DNA.

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Vogelgsang, Lars, Azlan Nisar, Sebastian Alexander Scharf, Anna Rommerskirchen, Dana Belick, Alexander Dilthey, and Birgit Henrich. "Characterisation of Type II DNA Methyltransferases of Metamycoplasma hominis." Microorganisms 11, no. 6 (June 15, 2023): 1591. http://dx.doi.org/10.3390/microorganisms11061591.

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Bacterial virulence, persistence and defence are affected by epigenetic modifications, including DNA methylation. Solitary DNA methyltransferases modulate a variety of cellular processes and influence bacterial virulence; as part of a restriction-modification (RM) system, they act as a primitive immune system in methylating the own DNA, while unmethylated foreign DNA is restricted. We identified a large family of type II DNA methyltransferases in Metamycoplasma hominis, comprising six solitary methyltransferases and four RM systems. Motif-specific 5mC and 6mA methylations were identified with a tailored Tombo analysis on Nanopore reads. Selected motifs with methylation scores >0.5 fit with the gene presence of DAM1 and DAM2, DCM2, DCM3, and DCM6, but not for DCM1, whose activity was strain-dependent. The activity of DCM1 for CmCWGG and of both DAM1 and DAM2 for GmATC was proven in methylation-sensitive restriction and finally for recombinant rDCM1 and rDAM2 against a dam-, dcm-negative background. A hitherto unknown dcm8/dam3 gene fusion containing a (TA) repeat region of varying length was characterized within a single strain, suggesting the expression of DCM8/DAM3 phase variants. The combination of genetic, bioinformatics, and enzymatic approaches enabled the detection of a huge family of type II DNA MTases in M. hominis, whose involvement in virulence and defence can now be characterized in future work.

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Okitsu, Cindy Yen, and Chih-Lin Hsieh. "DNA Methylation Dictates Histone H3K4 Methylation." Molecular and Cellular Biology 27, no. 7 (January 22, 2007): 2746–57. http://dx.doi.org/10.1128/mcb.02291-06.

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ABSTRACT Histone lysine methylation and DNA methylation contribute to transcriptional regulation. We have previously shown that acetylated histones are associated with unmethylated DNA and are nearly absent from the methylated DNA regions by using patch-methylated stable episomes in human cells. The present study further demonstrates that DNA methylation immediately downstream from the transcription start site has a dramatic impact on transcription and that DNA methylation has a larger effect on transcription elongation than on initiation. We also show that dimethylated histone H3 at lysine 4 (H3K4me2) is depleted from regions with DNA methylation and that this effect is not linked to the transcriptional activity in the region. This effect is a local one and does not extend even 200 bp from the methylated DNA regions. Although depleted primarily from the methylated DNA regions, the presence of trimethylated histone H3 at lysine 4 (H3K4me3) may be affected by transcriptional activity as well. The data here suggest that DNA methylation at the junction of transcription initiation and elongation is most critical in transcription suppression and that this effect is mechanistically mediated through chromatin structure. The data also strongly support the model in which DNA methylation and not transcriptional activity dictates a closed chromatin structure, which excludes H3K4me2 and H3K4me3 in the region, as one of the pathways that safeguards the silent state of genes.

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Wang, Heng, Yumo Xie, Gaopo Xu, Xiaolin Wang, Meijin Huang, Yanxin Luo, and Huichuan Yu. "Abstract 5272: Aberrant DNA 5mC and 6mA methylations increase ACE2 expression in intestinal cancer cells susceptible to SARS-CoV-2 infection." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5272. http://dx.doi.org/10.1158/1538-7445.am2022-5272.

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Abstract Angiotensin converting enzyme II (ACE2) is the cellular receptor of SARS-CoV-2. At present, ACE2 receptor is considered to be the key component in the SARS-CoV-2 infection and transmitting in the host. Among the cancer patients with COVID-19, the gastrointestinal cancer is the second most prevalent. The MethyLight and QASM assays were used to evaluated the genomic DNA 5mC methylation, while the CviAII enzyme-based 6mA-RE-qPCR was applied to determine motif-specific DNA 6mA methylation. The 6mA and 5mC methylation analyses of the long interspersed nuclear elements 1 (LINE1) were used to evaluate the global level of genomic 6mA and 5mC methylations, respectively. To investigate the role of ACE2 DNA methylation in regulating ACE2 expression, we performed a genome-wide methylation analysis in colorectal cancer samples collected at the Sixth Affiliated Hospital of Sun Yat-sen University. The DNA 5mC methylation of ACE2 promoter in tumor tissues were significantly lower than that in normal tissues, while the DNA 6mA methylation of ACE2 promoter in tumor tissues was significantly higher than that in normal tissues. In addition, the mRNA and protein expression of ACE2 in tumor tissues were lower than that in normal tissues. To explore the epigenetic regulation on ACE2 expression, we treated colon cancer cell lines with 5-Azacytidine and found ACE2 expression was upregulated after lowering the DNA 5mC methylation. The correlation analysis in patient cohort samples showed that ACE2 mRNA expression was positively correlated with DNA 5mC and negatively associated with DNA 6mA methylation. Next, a novel CRISPR-based tool was developed for sequence-specific 6mA editing on ACE2 promoter region, and it was applied in HCT116 cell to further confirm the regulatory role of DNA 6mA methylation in ACE2 mRNA expression. This tool was proved to be reliable with our findings that the CRISPR/dCas9-METTL3 tool could dramatically upregulate DNA 6mA methylation in ACE2 promoter, while the global level of genomic 6mA methylation remained unchanged. Both the mRNA and protein expression of ACE2 were significantly increased following a sequence-specific DNA 6mA editing in ACE2 promoter. In conclusion, we revealed the aberrant DNA 5mC and 6mA methylations in colorectal cancer, which upregulate ACE2 expression in colorectal cancer cells that may confer the susceptibility to SARS-CoV-2 infection. We developed a novel CRISPR-based tool that could realize site-directed 6mA methylation editing. Notably, the epigenetic regulation of DNA 6mA methylation on ACE2 expression provides an insight into the intersection of the biology of cancer, SARS-CoV-2 infection and organ-specific complication in COVID-19. Aberrant ACE2 methylation may serve as a biomarker and treatment target in these patients. Citation Format: Heng Wang, Yumo Xie, Gaopo Xu, Xiaolin Wang, Meijin Huang, Yanxin Luo, Huichuan Yu. Aberrant DNA 5mC and 6mA methylations increase ACE2 expression in intestinal cancer cells susceptible to SARS-CoV-2 infection [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5272.

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Majchrzak-Celińska, A., M. Naskret-Barciszewska, M. Giel-Pietraszuk, W. Nowak, P. Śron, and A. Barciszewska. "P02.08.A The relations of focal and total DNA methylation in gliomas." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii31. http://dx.doi.org/10.1093/neuonc/noac174.101.

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Abstract Background The role of epigenetic events in gliomagenesis is undoubtful. However, the role of specific pathological events is not so clear. It was shown that loss in total DNA methylation correlates with higher tumor malignancy and oxidative DNA damage. But promoter methylation of many genes was reported to be significant for gliomas’ malignancy and predictive for the treatment outcome. In carcinogenesis in general global DNA hypomethylation and focal hypermethylation coexist. The aim of our project was to evaluate the correlation between total DNA methylation and promoter methylation of selected genes. Material and Methods We analysed glioma tissues from 60 patients. For total DNA methylation analysis we used the radiolabelling method with TLC separation of nucleotides and content estimation with phosphoimager. For promoter methylation analysis we have chosen: MGMT (O-6-Methylguanine-DNA Methyltransferase), MPG (DNA-3-methyladenine glycosylase), GJA1 (Gap junction alpha-1 protein / connexin 43). The promoter methylation level was evaluated with the methylation-sensitive high-resolution melting (MS-HRM) method. Results Total DNA methylation was reversely correlated with brain tumor grade, confirming that 5-methylcytosine loss is important step in gliomagenesis. From 3 genes only MPG promoter methylation showed clear low reverse correlation with tumor grade. Promoter methylation in GJA1 show low correlation with both, MGMT and MPG, but there was no link between MGMT and MPG. IDHwt presence was significantly correlated with higher tumor grade. Promoter methylations in MPG and GJA1 were better correlated with IDH status than in MGMT. Conclusion There is a clear correlation between total DNA methylation and tumor malignancy. Gene promoter methylation is not highly correlated with total DNA methylation and shows low significance in selected cases. Promoter methylation showed clear correlation with tumor grade only in MPG case. That suggests diverse mechanisms steering DNA methylation in general and local changes. It also shows that total DNA methylation is best predictor of tumor grade.

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Dissertations / Theses on the topic "DNA methylation"

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Tasanasuwan, Piyama. "Targeted DNA methylation." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251476.

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MacLeod, A. Robert (Robert Alan) 1966. "DNA methylation and oncogenesis." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39956.

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DNA methylation is a postreplicative covalent modification of the DNA which is catalysed by the DNA methyltransferase enzyme. DNA methylation plays an important role in controlling the gene expression profile of mammalian cells. The hypothesis presented in this thesis is that the expression of the DNA methyltransferase gene is upregulated by cellular oncogenic pathways, and that this induction of MeTase activity results in DNA hypermethylation and plays a causal role in cellular transformation. Novel DNA methyltransferase inhibitors may inhibit the excessive activity of DNA methyltransferase in cancer cells and induce the original cellular genetic program. These inhibitors may also be used to turn on alternative gene expression programs. Therefore specific DNA methyltransferase antagonists might provide us with therapeutics directed at a nodal point in the regulation of genetic information.

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Tavares, de Araujo Felipe. "DNA replication and methylation." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37847.

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One of the main questions of modern biology is how our cells interpret our genetic and epigenetic information. DNA methylation is a covalent modification of the genome that is essential for mammalian development and plays an important role in the control of gene expression, genomic imprinting and X-chromosome inactivation (Bird and Wolffe, 1999; Szyf et al., 2000). Furthermore, changes in DNA methylation and DNA methyltransferase 1 (DNMT1) activity have been widely documented in a number of human cancers (Szyf, 1998a; Szyf et al., 2000).
In Escherichia coli, timing and frequency of initiation of DNA replication are controlled by the levels of the bacterial methyltransferase and by the methylation status of its origin of replication (Boye and Lobner-Olesen, 1990; Campbell and Kleckner, 1990). In mammalian cells, however, the importance of methyltransferase activity and of DNA methylation in replication is only now starting to emerge (Araujo et al., 1998; Delgado et al., 1998; DePamphilis, 2000; Knox et al., 2000).
The work described in this thesis focuses mainly on understanding the functional relationship between changes in DNA methylation and DNMT1 activity on mammalian DNA replication. In higher eukaryotes, DNA replication initiates from multiple specific sites throughout the genome (Zannis-Hadjopoulos and Price, 1999). The first part of the thesis describes the identification and characterization of novel in vivo initiation sites of DNA replication within the human dnmt1 locus (Araujo et al., 1999). Subsequently, a study of the temporal relationship between DNA replication and the inheritance of the DNA methylation pattern is presented. We also demonstrate that mammalian origins of replication, similarly to promoters, are differentially methylated (Araujo et al., 1998). We then tested the hypothesis that DNMT1 is a necessary component of the replication machinery. The results presented indicate that inhibition of DNMT1 results in inhibition of DNA replication (Knox et al., 2000). Finally, results are presented, demonstrating that the amino terminal region of DNMT1 is responsible for recognizing hemimethylated CGs, DNMT1's enzymatic target. Taken together, the results presented in this thesis demonstrate that DNMT1 is necessary for proper DNA replication and that DNA methylation may modulate origin function.

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Tsusaka, Takeshi. "Methylation of DNA Ligase 1 by G9a/GLP Recruits UHRF1 to Replicating DNA and Regulates DNA Methylation." Kyoto University, 2018. http://hdl.handle.net/2433/232305.

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Wong, Nicholas Chau-Lun. "DNA methylation at the neocentromere /." Connect to thesis, 2006. http://eprints.unimelb.edu.au/archive/00001883.

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Carrió, Gaspar Elvira. "DNA Methylation Dynamics during Myogenesis." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/296312.

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Myogenesis is the differentiation process which encompasses the formation of skeletal muscle during development, regeneration and tissue homeostasis throughout life. Arising from embryonic or adult stem cells, the myogenic process comprehends the acquisition of a specialized cell identity and the loss of pluri/multipotent and proliferative capacities. Starting with the hypothesis that DNA methylation, together with other epigenetic mechanisms and the transcription factors, orchestrates the transcriptional program, this thesis provides a comprehensive picture of DNA methylation dynamics during murine myogenic progression, addresses their regulatory implications, and identifies relevant differentially methylated regions that define muscle cell identity. Initially, we performed a genome-scale DNA methylation study comparing embryonic stem cells (ESCs), primary myoblasts (MBs), differentiated myotubes (MTs), and mature myofibers (MFs) using AIMS-seq method. We identified 1,000 differentially methylated regions during muscle-lineage determination and terminal differentiation, mainly located in gene bodies and intergenic regions. As a whole, muscle lineage commitment was characterized by a major gain of DNA methylation, while muscle differentiation was accompanied by loss of DNA methylation in CpG-poor regions. Notably, hypomethylated sequences were enriched in enhancer-type chromatin regions, suggesting the involvement of DNA methylation in the regulation of cell-type specific enhancers. Importantly, we detected a demethylated region overlapping the super-enhancer of the cell-identity factor Myf5. We showed that the activation of My5 super-enhancer took place upon DNA demethylation exclusively in muscle-committed cells resulting in gene expression. ChIP analyses showed that the binding of the Upstream stimulatory factor 1 (Usf1) to Myf5 locus was DNA demethylation-dependent in myogenic committed cells. Moreover, Usf1 binding site contained an embedded CpG conserved in humans and demethylated in human MBs but not in human ESCs, altogether reinforcing the hypothesis that DNA methylation regulates gene expression by modulating transcription factor binding accessibility. Next, we analyzed by sodium bisulphite sequencing the DNA methylation state of reported regulatory regions (with and without CpG island) of key genes implicated in myogenesis. After analyzing myogenic and non-myogenic cells we concluded that the muscle cell identity comprehends DNA demethylation of lineage-specific CpG-poor regulatory regions leading to a transcriptionally poised or activated state, while myogenic CpG island promoters are totally unmethylated during myogenesis and are regulated by histone modifications. A collaborative work with Charles Keller’s Lab (Oregon Health & Science University, USA) allowed us to conclude that Rhabdomyosarcoma cell lines present a spurious methylation pattern at usually unmethylated CpG islands, consequently with the aberrant methylation associated to tumorigenesis. Furthermore, the study of pluripotency gene promoters during myogenesis pointed that CpG-poor promoters are repressed during differentiation by DNA methylation and by Polycomb complex at CpG island promoters. Interested in deepen in the DNA demethylation dynamics, we started a collaboration with Rita Perlingeiro’s Lab (University of Minnesota, USA) to study the DNA methylation changes in the myogenic inducible Pax7 ESC-derived model. We showed that the ESC-derived myoblast precursors recreated the DNA methylation signature of in vivo isolated muscle stem cells, supporting this model as a bona fide strategy to generate myogenic precursors in vitro with therapeutic purposes. Finally, we addressed the involvement of an active demethylating mechanism during myogenesis. Apobec2 down-regulation in inducible ESC-derived myoblast precursors with shRNA strategies affected dramatically the myogenic differentiation by impairing DNA demethylation of the Myogenin promoter and abolishing the expression of Myogenin and MHC proteins. Based on these results, we proposed that Apobec2 might be involved in the active muscle specific DNA demethylation along myogenesis.
Partint de la hipòtesi que la metilació de l’ADN, junt amb altres mecanismes epigenètics i els factors de transcripció, orquestra el programa transcripcional, aquesta tesi ofereix un estudi exhaustiu de les dinàmiques de l'ADN durant la progressió miogènica, aborda les seves possibles implicacions reguladores i identifica regions diferencialment metilades que defineixen la identitat de la cèl·lula muscular. L’anàlisi a escala genòmica els perfils de metilació en diferents estadis de la miogènesi va permetre identificar 1000 regions diferencialment metilades, localitzades principalment en regions intergèniques i intragèniques. La majoria de canvis observats eren guanys de metilació i ocorrien durant la determinació de llinatge. D’altra banda, certes regions amb perfils de cromatina associats a enhancers esdevenien desmetilades, suggerint que la metilació de l’ADN pot estar implicada en la regulació de enhancers específics de teixit. L’estudi de gens específics de múscul va mostrar que la identitat de la cèl·lula muscular requereix la desmetilació de l'ADN de regions reguladores pobres en CpGs, alhora que els gens miogènics amb illes CpG a la regió promotora es troben sempre desmetilats i són regulats per modificacions d’histones. Un exemple de la desmetilació específica de múscul és la regió super-enhancer de Myf5. Els assajos d'immunoprecipitació de la cromatina van demostrar que la unió del factor de transcripció Usf1 al locus Myf5 només es donava quan l’ADN estava desmetilat, reforçant la hipòtesi que la metilació de l'ADN regula l'expressió gènica mitjançant la modulació de l'accessibilitat dels factors de transcripció al seu lloc d’unió. Mitjançant l’estudi el perfil de metilació de l'ADN de gens miogènics en un model miogènic derivat de cèl·lules embrionàries, es va observar el mateix perfil observat en mioblasts primaris, indicant que aquest model és una bona estratègia per obtenir mioblasts in vitro amb finalitats terapèutiques. Finalment, el bloqueig de la deaminasa Apobec2 va afectar severament la diferenciació miogènica i la desmetilació de l'ADN del promotor de la Miogenina, indicant que la deaminasa Apobec2 podria estar implicada en la desmetilació activa de l'ADN.

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Akman, Kemal. "Bioinformatics of DNA Methylation analysis." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-182873.

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陳桂儀 and Kwai-yi Jacqueline Chan. "DNA methylation and pediatric cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970370.

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Ó, Riain Ciarán Liam. "DNA methylation in follicular lymphoma." Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1318.

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Follicular Lymphoma (FL) is a common B cell Non-Hodgkin Lymphoma with a median survival of 8-10 years. Patients frequently undergo transformation to a more aggressive lymphoma and this is associated with drastically reduced survival. The hallmark of FL is the t(14;18) translocation yet this alone is insufficient for lymphomagenesis. While a number of secondary genetic changes have been described, epigenetic studies have lagged behind. Epigenetics refers to mechanisms that alter gene expression without a change in the primary DNA sequence. DNA methylation was quantitatively profiled at 1505 CpG loci in 164 untreated FL as well as 10 pairs of pre- and post-transformation samples and 24 benign haematopoietic controls. Tumour-specific methylation occurred in >100 genes, preferentially occurring within CpG rich areas known as CpG islands and in genes marked by a repressive histone modification in embryonic stem (ES) cells, trimethylated Lysine 27 of Histone H3 (H3K27Me3). Significant inverse correlation with gene expression was identified for a small number of genes. Significant changes in methylation were not seen in FL samples upon transformation. These findings suggested that widespread DNA methylation occurred as an early 'pre-programmed' event in lymphomagenesis rather than being due to silencing of individual tumour suppressor genes. Methylation profiling of a subset of these samples at >27,000 CpG loci revealed aberrant methylation in FL in >700 CpG islands. These hypermethylated genes were enriched for high-density CpG promoters and for a key set of genes with developmental function which were marked by both repressive (H3K27Me3) and activating (H3K4Me3) marks in ES cells. Examination of H3K27me3 expression by immunohistochemistry in pre- and post-transformation biopsy samples showed wide variation in expression. Furthermore, mutations were identified in the histone methylase EZH2 that catalyses H3K27Me3, in 7 of 20 patients. We can conclude therefore that deregulation of DNA and histone methylation are critical inter-related events for FL pathogenesis.

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Gonçalves, Athanásio Camila. "DNA methylation in Daphnia magna." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/7140/.

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Daphnia magna is gaining interest as a model for epigenetic research. It is easy to maintain under laboratory conditions and has low genetic diversity due to parthenogenetic reproduction. The D. magna genome is responsive to a wide range of stimuli and genomics resources are being developed for this species. Despite these great advantages, information regarding the epigenome of D. magna and its regulation is still lacking. Thus, the main aim of this work was to describe the methylome of D.magna and investigate its regulation and responsiveness to environmentally relevant exposure conditions. Despite the low levels of global DNA methylation, a defined profile could be identified. DNA methylation in D. magna is sporadic and mainly found at coding regions. These data suggest that D. magna encodes a complete set of genes for DNA methylation reactions. Evidence of direct effects on the DNA methylation profile were found in animals exposed to the DNA methylation inhibitor 5-azacytidine and these changes were persistent after the removal of the stressor. Acute and chronic exposures to environmentally relevant concentrations of stressors (arsenic and hypoxia) also induced changes in gene transcription levels and concentrations of onecarbon pathway metabolites. These findings indicate that the epigenome of D. magna is responsive to changes in the environment, supporting its use as an environmentally relevant model organism for epigenetics research. Furthermore, the maintenance of some of the epigenetic changes in the absence of the initial stressor supports the concept of ‘epigenetic memory’ and its potential use in chemical risk assessment.

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Books on the topic "DNA methylation"

1

Jost, Jean-Pierre, and Hans-Peter Saluz, eds. DNA Methylation. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9.

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Tost, Jörg, ed. DNA Methylation. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-522-0.

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Mills, Ken I., and Bernie H. Ramsahoye. DNA Methylation Protocols. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592591825.

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Tost, Jörg, ed. DNA Methylation Protocols. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7481-8.

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5

I, Mills Ken, and Ramsahoye Bernie H, eds. DNA methylation protcols. Totowa, N.J: Humana Press, 2002.

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6

B, Kobayashi Taku, ed. DNA methylation research trends. Hauppauge, N.Y: Nova Science Publishers, 2007.

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7

Vani︠u︡shin, B. F. DNA methylation in plants. New York: Nova Science Publishers, Inc., 2008.

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Doerfler, Walter, and Petra Böhm, eds. DNA Methylation: Basic Mechanisms. Berlin/Heidelberg: Springer-Verlag, 2006. http://dx.doi.org/10.1007/3-540-31390-7.

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Jones, Peter A., and Peter K. Vogt, eds. DNA Methylation and Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59696-4.

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H, Burdon R., ed. Molecular biology of DNA methylation. New York: Springer-Verlag, 1985.

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Book chapters on the topic "DNA methylation"

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Weissbach, Arthur. "A Chronicle of DNA methylation (1948–1975)." In DNA Methylation, 1–10. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_1.

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Selker, Eric U. "Control of DNA methylation in fungi." In DNA Methylation, 212–17. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_10.

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Finnegan, E. J., R. I. S. Brettell, and E. S. Dennis. "The role of DNA methylation in the regulation of plant gene expression." In DNA Methylation, 218–61. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_11.

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Doerfler, Walter. "Patterns of de novo DNA methylation and promoter inhibition: Studies on the adenovirus and the human genomes." In DNA Methylation, 262–99. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_12.

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Bednarik, Daniel P. "DNA Methylation and retrovirus expression." In DNA Methylation, 300–329. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_13.

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Rachal, Mack J., Paula Holton, and Jean-Numa Lapeyre. "Effect of DNA methylation on dynamic properties of the helix and nuclear protein binding in the H-ras promoter." In DNA Methylation, 330–42. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_14.

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Razin, Aharon, and Howard Cedar. "DNA methylation and embryogenesis." In DNA Methylation, 343–57. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_15.

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Singer-Sam, Judith, and Arthur D. Riggs. "X chromosome inactivation and DNA methylation." In DNA Methylation, 358–84. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_16.

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Chu, Chien, and C. K. James Shen. "DNA methylation: Its possible functional roles in developmental regulation of human globin gene families." In DNA Methylation, 385–403. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_17.

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Graessmann, M., and A. Graessmann. "DNA Methylation, chromatin structure and the regulation of gene expression." In DNA Methylation, 404–24. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_18.

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Conference papers on the topic "DNA methylation"

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Diaz-Blanco, Ignacio, Jose M. Enguita-Gonzalez, Diego Garcia-Perez, Abel A. Cuadrado-Vega, Nuria Valdes-Gallego, and Maria Dolores Chiara-Romero. "Analysis of DNA methylation patterns in cancer samples using SOM." In ESANN 2024, 715–20. Louvain-la-Neuve (Belgium): Ciaco - i6doc.com, 2024. http://dx.doi.org/10.14428/esann/2024.es2024-42.

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Son, Joo-Hiuk. "Active Demethylation of Cancer Cells using Terahertz Radiation for Potential Cancer Treatment." In Conference on Lasers and Electro-Optics/Pacific Rim. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleopr.2022.cmp3a_02.

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Carcinogenesis involves DNA methylation which is a primary alteration in DNA in the development of cancer before genetic mutation. Because the abnormal DNA methylation is found in most cancer cells, the assessment of DNA methylation using terahertz radiation can be a novel optical method to detect and control cancer. The methylation has been directly observed by terahertz time-domain spectroscopy and this epigenetic chemical change could be manipulated to the state of demethylation using resonant terahertz radiation. Demethylation of cancer cells is a key issue in epigenetic cancer therapy and our results may lead to the treatment of cancer using electromagnetic waves.

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"Unlocking DNA methylation with BSXplorer." In Биоинформатика регуляции и структуры геномов / системная биология. ИЦиГ СО РАН, 2024. http://dx.doi.org/10.18699/bgrs2024-1.2-25.

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Hagestedt, Inken, Mathias Humbert, Pascal Berrang, Irina Lehmann, Roland Eils, Michael Backes, and Yang Zhang. "Membership Inference Against DNA Methylation Databases." In 2020 IEEE European Symposium on Security and Privacy (EuroS&P). IEEE, 2020. http://dx.doi.org/10.1109/eurosp48549.2020.00039.

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Jing, Jian, Elizabeth Davidson, Brent Pedersen, Daniel LaFlamme, Ivana V. Yang, and David A. Schwartz. "DNA Methylation And Innate Immune Tolerance." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1367.

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Carvalho, GFS, LL Vieira, BM Wolff, YG Oliveira, VT Almeida, AM Nascimento, and LD Kulikowski. "EPIGENOMIC ANALYSIS REVEAL CRITICAL ASSOCIATION BETWEEN METHYLATION STATUS AND CLINICAL PHENOTYPE." In Resumos do 54º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial, 24–25. Zeppelini Editorial e Comunicação, 2022. http://dx.doi.org/10.5327/1516-3180.140s1.5803.

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Objective: Copy number variations (CNVs) are DNA fragments deleted or duplicated in relation to a reference genome. Some genome variants, classified as variants with uncertain significance (VUS), do not present a safe conclusion with clinical phenotypes, which makes the diagnostic conclusion difficult. We know that hypermethylation of gene promoter regions often leads to transcriptional silencing, in addition to DNA methylation changes in gene and/or intergenic regions can play a critical role in genomic regulation and stability. With epigenomic investigation, we can gain a more comprehensive understanding of the modulation in gene expression associated with genomic imbalance in different diseases and in different genomic variations. So, our objective is to understand the impact of methylation status associated with genomic imbalances in clinical phenotypes. Method: Our study evaluated, using the Infinium Methylation EPIC Bead Chip platform, 10 DNA samples from patients with intellectual disability and dysmorphic features with CNVs classified as VUS without a definitive clinical diagnosis, in addition to six control samples from participants without clinical conditions. Conclusion: Genomic methylation, associated with genomic structural imbalances, can play a critical role in clinical features and can be used as an important marker for patients with uncertain clinical diagnosis.

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Almeida, V., SN Chehimi, GFS Carvalho, YG Oliveira, AM Nascimento, LL Vieira, BM Wolff, and LD Kulikowski. "DIFFERENCE IN METHYLATION STATUS OF REMAINING ALLELE IN SIBLINGS WITH THE SAME DELETION SIZE IN 5P." In Resumos do 54º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial, 42. Zeppelini Editorial e Comunicação, 2022. http://dx.doi.org/10.5327/1516-3180.140s1.6429.

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Objective: Cri Du Chat syndrome or 5psyndrome (OMIM #123450) is characterized by a genomic loss in the short arm of chromosome 5 and by variable clinical manifestations, that include high-pitched cry in newborns. The phenotypic variability in this syndrome may not be limited only to variations in gene structure – such as deletions, duplications, inversions, insertions and translocations – as DNA methylation mechanisms, which occurs mainly in the “CpG Islands”, are also possible. Therefore, we studied the methylation status of the remaining allele of region of breakpoint at 5pin siblings, an 11-year-old boy and a 13-year-old girl, with a same size deletion inherited from their mother and with distinct phenotypes. Method: DNA samples from siblings with the same deletion size in 5p delimited by genomic array were evaluated using the Infinium Human Methylation 450 BeadChip platform. The bioinformatics analysis was performed in R programming language. Conclusion: We noticed a difference in methylation status of the remaining allele at the breakpoint of region of 5pin the siblings. We infer that this difference in methylation may explain the phenotypic differences in patients with this syndrome.

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Kanae, Haruki, Terumasa Ito, Kaori Tsukakoshi, Shintaro Inaba, Mizuki Tomizawa, Kaustav Das, Kazunori Ikebukuro, and Kazuhiko Misawa. "Detection of structural changes in DNA due to methylation using Raman spectroscopy." In Optical Tomography and Spectroscopy. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/ots.2024.ow1d.4.

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Steric conformational changes in the guanine quadruplex (G4) structure due to DNA methylation are associated with cancer. We show that Raman spectroscopy can be used to detect the conformational changes in the G4 structure.

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Kulikowski, LD, G. Carvalho, YG Oliveira, TVMM Costa, LL Vieira, VT Almeida, and A. Nascimento. "METHYLATION AND BIOLOGICAL AGE ANALYSIS IN ADHD PATIENTS." In Resumos do 54º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial, 41–42. Zeppelini Editorial e Comunicação, 2022. http://dx.doi.org/10.5327/1516-3180.140s1.5854.

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Objective: Attention deficit/hyperactivity disorder (ADHD) is a common behavioral syndrome that begins in childhood and affects 3.4% of children worldwide. Due to its etiological complexity, there are no consistent biomarkers for ADHD, however the high heritability that the disorder presents indicates an influence of genetic/ epigenetic factors. The main epigenetic mechanisms is DNA methylation, a process with an important role in gene expression and in many biological pathways. Methylation status can be used as a biomarker for clinical conditions, such as cancer and neuropsychiatric diseases with specific epi-signatures, and it is used as a marker of biological senescence by several studies to determine biological age (DNAmAge). Thus, our study sought to identify epi-signatures biomarkers in 29 children clinically diagnosed with ADHD. Method: We using the Infinium Human Methylation 450 platform BeadChip (Illumina) and a pipeline of bioinformatics analysis in R programming language.To obtain biological ages through epigenetic marker. Conclusion: The results highlight the interaction of energy metabolism and oxidative stress pathways in ADHD patients detected by differential methylation patterns. We were able to identify a marginal association between the DNAmAge and ADHD. Thus, we present new methylation biomarkers in ADHD patients and propose that further multiethnic studies with larger cohorts should be done to demonstrate a definitive association between ADHD and these methylation biomarkers. References: 1. Schuch V, Utsumi DA, Costa TVMM, Kulikowski LD, Muszkat M. Attention déficit hyperactivity disorder in the light of the epigenetic paradigm. Front Psychiatry. 2015; 6: 126. 2. Pelegí-Sisó D, de Prado P, Ronkainen J, Bustamante M, González JR. Methylclock: a bioconductor package to estimate DNA methylation age. Bioinformatics. 2021; 37(12): 1759-60.

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Zheng, Kai, Hanzhe Liu, Simin Zhu, Huamei Li, and Xiaozhou Chen. "DNA Methylation Analysis Methods for Cancer Research." In 5th International Conference on Information Engineering for Mechanics and Materials. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/icimm-15.2015.188.

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Reports on the topic "DNA methylation"

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Muyle, Aline. Analysis of DNA Methylation. Instats Inc., 2024. http://dx.doi.org/10.61700/6ayq8hff26qxn1470.

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This three-day workshop provides comprehensive training in the analysis of DNA methylation, a key epigenetic modification influencing gene expression and controlling the spread of transposable elements in genomes. Led by Dr Aline Muyle, participants will gain theoretical knowledge and practical skills in data preprocessing, statistical analysis, and visualization using RStudio and various bioinformatic software using Bash scripts. The workshop is suited for researchers in Biostatistics, Biology, Genetics, Ecology, Evolution, Bioinformatics, Molecular Biology, and Medical Research.

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Head, Thomas J., and Susannah Gal. DNA Based Fluid Computing Using Methylation. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada436701.

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Yamamoto, Fumiichiro. DNA Methylation Alterations in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada405531.

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Yamamoto, Fumiichiro. DNA Methylation Alterations in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408999.

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Cullen, Kevin J. The Effect of DNA Methylation on IGF2 Expression. Fort Belvoir, VA: Defense Technical Information Center, September 1998. http://dx.doi.org/10.21236/ada361324.

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Huang, Tim H. M. Epigenetic Changes in DNA methylation in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada384184.

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Repository, Science. Epigenetics – Blurring the Lines between Nature and Nurture. Science Repository OÜ, November 2020. http://dx.doi.org/10.31487/sr.blog.12.

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Singal, Rakesh. Aberrant Promoter Methylation in Serium DNA as a Biomarker for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada452528.

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Rusiecki, Jennifer A., Louis French, Zygmunt Galdzicki, Celia Byrne, Ligong Chen, Liying Yan, and Matthew Polin. Epigenetic Patterns of TBI: DNA Methylation in Serum of OIF/OEF Servicemembers. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada585498.

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Rusiecki, Jennifer A. Epigenetic Patterns of TBI: DNA Methylation in Serum of OIF/OEF Service Members. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada540727.

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