Thematische Bibliographien / Site-specific DNA methylation

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Auswahl der wissenschaftlichen Literatur zum Thema „Site-specific DNA methylation“

Autor: Grafiati

Veröffentlicht am 25. Mai 2024

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Zeitschriftenartikel zum Thema "Site-specific DNA methylation"

Choudhury, Samrat Roy, Yi Cui, Anoop Narayanan, et al. "Optogenetic regulation of site-specific subtelomeric DNA-methylation." Oncotarget 7, no. 31 (2016): 50380–91. http://dx.doi.org/10.18632/oncotarget.10394.

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Stains, Cliff I., Jennifer L. Furman, David J. Segal, and Indraneel Ghosh. "Site-Specific Detection of DNA Methylation Utilizing mCpG-SEER." Journal of the American Chemical Society 128, no. 30 (2006): 9761–65. http://dx.doi.org/10.1021/ja060681j.

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Bruce, Sara, Katariina Hannula-Jouppi, Cecilia M. Lindgren, Marita Lipsanen-Nyman, and Juha Kere. "Restriction Site–Specific Methylation Studies of Imprinted Genes with Quantitative Real-Time PCR." Clinical Chemistry 54, no. 3 (2008): 491–99. http://dx.doi.org/10.1373/clinchem.2007.098491.

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Abstract Background: Epigenetic studies, such as the measurement of DNA methylation, are important in the investigation of syndromes influenced by imprinted genes. Quick and accurate quantification of methylation at such genes can be of appreciable diagnostic aid. Methods: We first digested genomic DNA with methylation-sensitive restriction enzymes and used DNA without digestion as a control and nonmethylated λ DNA as an internal control for digestion efficiency. We then performed quantitative real-time PCR analyses with 6 unique PCR assays to investigate 4 imprinting control regions on chromosomes 7 and 11 in individuals with uniparental disomy of chromosome 7 (UPD7) and in control individuals. Results: Our validation of the method demonstrated both quantitative recovery and low methodologic imprecision. The imprinted loci on chromosome 7 behaved as expected in maternal UPD7 (100% methylation) and paternal UPD7 (&lt;10% methylation). In controls, the mean (SD) for percent methylation at 2 previously well-studied restriction sites were 46% (6%) for both H19 and KCNQ1OT1, a result consistent with the previously observed methylation rate of approximately 50%. The methylation percentages of all investigated imprinted loci were normally distributed, implying that the mean and SD can be used as a reference for screening methylation loss or gain. Conclusion: The investigated loci are of particular importance for investigating the congenital Silver–Russell and Beckwith–Wiedemann syndromes; however, the method can also be applied to other imprinted regions. This method is easy to set up, has no PCR bias, requires small amounts of DNA, and can easily be applied to large patient populations for screening the loss or gain of methylation.

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Noack, Florian, Abhijeet Pataskar, Martin Schneider, Frank Buchholz, Vijay K. Tiwari, and Federico Calegari. "Assessment and site-specific manipulation of DNA (hydroxy-)methylation during mouse corticogenesis." Life Science Alliance 2, no. 2 (2019): e201900331. http://dx.doi.org/10.26508/lsa.201900331.

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Dynamic changes in DNA (hydroxy-)methylation are fundamental for stem cell differentiation. However, the signature of these epigenetic marks in specific cell types during corticogenesis is unknown. Moreover, site-specific manipulation of cytosine modifications is needed to reveal the significance and function of these changes. Here, we report the first assessment of (hydroxy-)methylation in neural stem cells, neurogenic progenitors, and newborn neurons during mammalian corticogenesis. We found that gain in hydroxymethylation and loss in methylation occur sequentially at specific cellular transitions during neurogenic commitment. We also found that these changes predominantly occur within enhancers of neurogenic genes up-regulated during neurogenesis and target of pioneer transcription factors. We further optimized the use of dCas9-Tet1 manipulation of (hydroxy-)methylation, locus-specifically, in vivo, showing the biological relevance of our observations for Dchs1, a regulator of corticogenesis involved in developmental malformations and cognitive impairment. Together, our data reveal the dynamics of cytosine modifications in lineage-related cell types, whereby methylation is reduced and hydroxymethylation gained during the neurogenic lineage concurrently with up-regulation of pioneer transcription factors and activation of enhancers for neurogenic genes.

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Murata, Mariko, Ayako Takahashi, Isao Saito, and Shosuke Kawanishi. "Site-specific DNA methylation and apoptosis: induction by diabetogenic streptozotocin." Biochemical Pharmacology 57, no. 8 (1999): 881–87. http://dx.doi.org/10.1016/s0006-2952(98)00370-0.

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Rajeevan, Mangalathu S., David C. Swan, Kara Duncan, Daisy R. Lee, Josef R. Limor, and Elizabeth R. Unger. "Quantitation of site-specific HPV 16 DNA methylation by pyrosequencing." Journal of Virological Methods 138, no. 1-2 (2006): 170–76. http://dx.doi.org/10.1016/j.jviromet.2006.08.012.

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Chang, Shujun, Clint W. Magill, Jane M. Magill, Franklin Fong, and Ronald J. Newton. "PCR amplification following restriction to detect site-specific DNA methylation." Plant Molecular Biology Reporter 10, no. 4 (1992): 362–66. http://dx.doi.org/10.1007/bf02668912.

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Dong, Zizheng, Xiaofu Wang, and B. Mark Evers. "Site-specific DNA methylation contributes to neurotensin/neuromedin N expression in colon cancers." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 6 (2000): G1139—G1147. http://dx.doi.org/10.1152/ajpgi.2000.279.6.g1139.

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The neurotensin/neuromedin N (NT/N) gene is expressed in fetal colon, repressed in newborn and adult colon, and reexpressed in ∼25% of colon cancers. Our purpose was to determine the effect of gene methylation on NT/N silencing in colon cancers. We found that the NT/N gene was expressed in human colon cancer cell line KM12C but not in KM20 colon cancer cells. Bisulfite genomic sequencing demonstrated that all CpG dinucleotides in the region from −373 to +100 of the NT/N promoter, including a CpG site in a distal consensus AP-1 site, were methylated in KM20 but unmethylated in KM12C cells. Treatment of KM20 cells with demethylating agent 5-azacytidine induced NT/N expression, suggesting a role for DNA methylation in silencing of NT/N in colon cancers. To better elucidate the mechanisms responsible for NT/N repression by DNA methylation, we performed gel shift assays using an oligonucleotide probe corresponding to the distal AP-1 consensus sequence of the NT/N promoter. Methylation of the oligonucleotide probe inhibited protein binding to the distal AP-1 site of the NT/N promoter, suggesting a potential mechanism of NT/N gene repression in colon cancers. We show that DNA methylation plays a role in NT/N gene silencing in the human colon cancer KM20 and that NT/N expression in KM12C cells is associated with demethylation of the CpG sites. DNA methylation likely contributes to NT/N gene expression noted in human colon cancers.

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Huang, Yung-Hsin, Su Jianzhong, Yong Lei, et al. "DNA Epigenome Editing Using Crispr-Cas Suntag-Directed DNMT3A." Blood 128, no. 22 (2016): 2707. http://dx.doi.org/10.1182/blood.v128.22.2707.2707.

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Abstract DNA methylation, an epigenetic modification, has widespread effects on gene expression during development. However, our ability to assign specific function to regions of DNA methylation is limited by the poor correlation between global patterns of DNA methylation and gene expression. To overcome this barrier, we utilized nuclease-deactivated Cas9 protein fused to repetitive peptide epitopes (SunTag) recruiting multiple copies of antibody-fused de novo DNA methyltranferase 3A (DNMT3A) (CRISPR-Cas SunTag-directed DNMT3A) to amplify local DNMT3A concentration and to methylate genomic sites of interest. Here, we demonstrated that CRISPR-Cas SunTag-directed DNMT3A not only dramatically increased CpG methylation but also, to our surprise, CpH (H =A or C or T) methylation at the HOXA5 lociin human embryonic kidney 293T cells (HEK293T). Furthermore, using a single sgRNA, CRISPR-Cas SunTag-directed DNMT3A was capable of methylating 4.5 kb genomic regions, surpassing previous targeted methylation tools whose activity is limited to 200bp. Using reduced representation bisulfite sequencing (RRBS) and RNA-seq, we concluded that CRISPR-Cas SunTag-directed DNMT3A methylated regions of interest without affecting global DNA methylome and transcriptome. This effective and precise tool enables site-specific manipulation of DNA methylation and may be used to address the relationship beteween DNA methylation and gene expression. Disclosures No relevant conflicts of interest to declare.

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Graessmann, A., G. Sandberg, E. Guhl, and M. Graessmann. "Methylation of single sites within the herpes simplex virus tk coding region and the simian virus 40 T-antigen intron causes gene inactivation." Molecular and Cellular Biology 14, no. 3 (1994): 2004–10. http://dx.doi.org/10.1128/mcb.14.3.2004-2010.1994.

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In order to determine whether partial methylation of the herpes simplex virus (HSV) tk gene prevents tk gene expression, the HSV tk gene was cloned as single-stranded DNA. By in vitro second-strand DNA synthesis, specific HSV tk gene segments were methylated, and the hemimethylated DNA molecules were microinjected into thymidine kinase-negative rat2 cells. Conversion of the hemimethylated DNA into symmetrical methylated DNA and integration into the host genome occurred early after gene transfer, before the cells entered into the S phase. HSV tk gene expression was inhibited either by promoter methylation or by methylation of the coding region. Using the HindIII-SphI HSV tk DNA fragment as a primer for in vitro DNA synthesis, all cytosine residues within the coding region, from +499 to +1309, were selectively methylated. This specific methylation pattern caused inactivation of the HSV tk gene, while methylation of the cytosine residues within the nucleotide sequence from +811 to +1309 had no effect on HSV tk gene activity. We also methylated single HpaII sites within the HSV tk gene using a specific methylated primer for in vitro DNA synthesis. We found that of the 16 HSV tk HpaII sites, methylation of 6 single sites caused HSV tk inactivation. All six of these "methylation-sensitive" sites are within the coding region, including the HpaII-6 site, which is 571 bp downstream from the transcription start site. The sites HpaII-7 to HpaII-16 were all methylation insensitive. We further inserted separately the methylation-sensitive HSV tk HpaII-6 site and the methylation-insensitive HpaII-13 site as DNA segments (32-mer) into the intron region of the simian virus 40 T antigen (TaqI site). Methylation of these HpaII sites caused inhibition of simian virus 40 T-antigen synthesis.

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