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Journal articles on the topic 'Site-specific DNA methylation'

Author: Grafiati

Published: 25 May 2024

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1

Choudhury, Samrat Roy, Yi Cui, Anoop Narayanan, David P. Gilley, Nazmul Huda, Chiao-Ling Lo, Feng C. Zhou, Dinesh Yernool, and Joseph Irudayaraj. "Optogenetic regulation of site-specific subtelomeric DNA-methylation." Oncotarget 7, no. 31 (July 4, 2016): 50380–91. http://dx.doi.org/10.18632/oncotarget.10394.

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2

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 (August 2006): 9761–65. http://dx.doi.org/10.1021/ja060681j.

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3

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 (March 1, 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 (<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 (February 27, 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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5

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

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6

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 (December 2006): 170–76. http://dx.doi.org/10.1016/j.jviromet.2006.08.012.

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7

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 (November 1992): 362–66. http://dx.doi.org/10.1007/bf02668912.

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8

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 (December 1, 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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9

Huang, Yung-Hsin, Su Jianzhong, Yong Lei, Michael C. Gundry, Xiaotian Zhang, Mira Jeong, Wei Li, and Margaret A. Goodell. "DNA Epigenome Editing Using Crispr-Cas Suntag-Directed DNMT3A." Blood 128, no. 22 (December 2, 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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10

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 (March 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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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 (March 1994): 2004–10. http://dx.doi.org/10.1128/mcb.14.3.2004.

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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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12

Grant, DJ, H. Shi, and CT Teng. "Tissue and site-specific methylation correlates with expression of the mouse lactoferrin gene." Journal of Molecular Endocrinology 23, no. 1 (August 1, 1999): 45–55. http://dx.doi.org/10.1677/jme.0.0230045.

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We have previously examined the regulatory region of the mouse lactoferrin gene and have identified sequences essential for basal and hormonally induced expression. In this study, we explore the relationship between the methylation state of the mouse lactoferrin gene promoter and its expression in selected mouse tissues. In a transient expression system, transcriptional activity was blocked after in vitro methylation of the regulatory region of the mouse lactoferrin gene. In addition, the in vivo methylation state of three promoter region sites was assessed using Southern blot analysis of DNA digested with methylation-insensitive and -sensitive restriction enzymes. The results showed that site -455, upstream of the mouse lactoferrin estrogen response module, was highly unmethylated in DNA from both hormone-treated and -untreated mouse lung, liver, and spleen tissues. Also, in both treated and untreated samples, the -54 site is uniquely highly unmethylated in liver DNA, while the -22 site is unmethylated in spleen DNA. Northern blot analysis showed lactoferrin expression in tissues that were unmethylated at a minimum of two sites. These results show that the alteration of the methylation status of the three sites are tissue-specific and are associated with constitutive expression of lactoferrin.

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13

ZHANG, ZHI-XIN, VIPIN KUMAR, RAY T. RIVERA, SALLY G. PASION, JANE CHISHOLM, and DEBAJIT K. BISWAS. "Suppression of Prolactin Gene Expression in GH Cells Correlates with Site-Specific DNA Methylation." DNA 8, no. 8 (October 1989): 605–13. http://dx.doi.org/10.1089/dna.1989.8.605.

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14

Nomura, Wataru, and Carlos F. Barbas. "In Vivo Site-Specific DNA Methylation with a Designed Sequence-Enabled DNA Methylase." Journal of the American Chemical Society 129, no. 28 (July 2007): 8676–77. http://dx.doi.org/10.1021/ja0705588.

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15

Tirosh, Amit, Jonathan Keith Killian, David Petersen, Yuelin Jack Zhu, Robert L. Walker, Jenny E. Blau, Naris Nilubol, et al. "Distinct DNA Methylation Signatures in Neuroendocrine Tumors Specific for Primary Site and Inherited Predisposition." Journal of Clinical Endocrinology & Metabolism 105, no. 10 (July 24, 2020): 3285–94. http://dx.doi.org/10.1210/clinem/dgaa477.

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Abstract Purpose To compare the deoxyribonucleic acid (DNA) methylation signature of neuroendocrine tumors (NETs) by primary tumor site and inherited predisposition syndromes von Hippel–Lindau disease (VHL) and multiple endocrine neoplasia type 1 (MEN1). Methods Genome-wide DNA methylation (835 424 CpGs) of 96 NET samples. Principal components analysis (PCA) and unsupervised hierarchical clustering analyses were used to determine DNA methylome signatures. Results Hypomethylated CpGs were significantly more common in VHL-related versus sporadic and MEN1-related NETs (P < .001 for both comparisons). Small-intestinal NETs (SINETs) had the most differentially methylated CpGs, either hyper- or hypomethylated, followed by duodenal NETs (DNETs) and pancreatic NETs (PNETs, P < .001 for all comparisons). There was complete separation of SINETs on PCA, and 3 NETs of unknown origin clustered with the SINET samples. Sporadic, VHL-related, and MEN1-related PNETs formed distinct groups on PCA, and VHL clustered separately, showing pronounced DNA hypomethylation, while sporadic and MEN1-related NETs clustered together. MEN1-related PNETs, DNETs, and gastric NETs each had a distinct DNA methylome signature, with complete separation by PCA and unsupervised clustering. Finally, we identified 12 hypermethylated CpGs in the 1A promoter of the APC (adenomatous polyposis coli) gene, with higher methylation levels in MEN1-related NETs versus VHL-related and sporadic NETs (P < .001 for both comparisons). Conclusions DNA CpG methylation profiles are unique in different primary NET types even when occurring in MEN1-related NETs. This tumor DNA methylome signature may be utilized for noninvasive molecular characterization of NETs, through DNA methylation profiling of biopsy samples or even circulating tumor DNA in the near future.

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16

Rao, B. S., and A. Buckler-White. "Direct visualization of site-specific and strand-specific DNA methylation patterns in automated DNA sequencing data." Nucleic Acids Research 26, no. 10 (May 1, 1998): 2505–7. http://dx.doi.org/10.1093/nar/26.10.2505.

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17

Han, Weiguo, Miao Shi, and Simon D. Spivack. "Site-specific methylated reporter constructs for functional analysis of DNA methylation." Epigenetics 8, no. 11 (November 2013): 1176–87. http://dx.doi.org/10.4161/epi.26195.

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18

McDonald, James I., Hamza Celik, Lisa E. Rois, Gregory Fishberger, Tolison Fowler, Ryan Rees, Ashley Kramer, Andrew Martens, John R. Edwards, and Grant A. Challen. "Reprogrammable CRISPR/Cas9-based system for inducing site-specific DNA methylation." Biology Open 5, no. 6 (May 11, 2016): 866–74. http://dx.doi.org/10.1242/bio.019067.

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19

Nelson, M., and M. McClelland. "Site-specific methylation: effect on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 19, suppl (April 25, 1991): 2045–71. http://dx.doi.org/10.1093/nar/19.suppl.2045.

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20

Healey, Matthew J., William Rowe, Sofia Siati, Muttuswamy Sivakumaran, and Mark Platt. "Rapid Assessment of Site Specific DNA Methylation through Resistive Pulse Sensing." ACS Sensors 3, no. 3 (March 7, 2018): 655–60. http://dx.doi.org/10.1021/acssensors.7b00935.

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21

Blattler, Adam, and Peggy J. Farnham. "Cross-talk between Site-specific Transcription Factors and DNA Methylation States." Journal of Biological Chemistry 288, no. 48 (October 22, 2013): 34287–94. http://dx.doi.org/10.1074/jbc.r113.512517.

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22

Ogushi, Shoko, Yuya Yoshida, Tsuyoshi Nakanishi, and Tomoki Kimura. "CpG Site-Specific Regulation of Metallothionein-1 Gene Expression." International Journal of Molecular Sciences 21, no. 17 (August 19, 2020): 5946. http://dx.doi.org/10.3390/ijms21175946.

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Metal-binding inducible proteins called metallothioneins (MTs) protect cells from heavy-metal toxicity. Their transcription is regulated by metal response element (MRE)-binding transcription factor-1 (MTF1), which is strongly recruited to MREs in the MT promoters, in response to Zn and Cd. Mouse Mt1 gene promoter contains 5 MREs (a–e), and MTF1 has the highest affinity to MREd. Epigenetic changes like DNA methylation might affect transcription and, therefore, the cytoprotective function of MT genes. To reveal the CpG site(s) critical for Mt1 transcription, we analyzed the methylation status of CpG dinucleotides in the Mt1 gene promoter through bisulfite sequencing in P1798 mouse lymphosarcoma cells, with high or low MT expression. We found demethylated CpG sites near MREd and MREe, in cells with high expression. Next, we compared Mt1 gene-promoter-driven Lucia luciferase gene expression in unmethylated and methylated reporter vectors. To clarify the effect of complete and partial CpG methylation, we used M.SssI (CG→5mCG) and HhaI (GCGC→G5mCGC)-methylated reporter vectors. Point mutation analysis revealed that methylation of a CpG site near MREd and MREe strongly inhibited Mt1 gene expression. Our results suggest that the methylation status of this site is important for the regulation of Mt1 gene expression.

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23

Bernstein, Carol. "DNA Methylation and Establishing Memory." Epigenetics Insights 15 (January 2022): 251686572110724. http://dx.doi.org/10.1177/25168657211072499.

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A single event can cause a life-long memory. Memories physically reside in neurons, and changes in neuronal gene expression are considered to be central to memory. Early models proposed that specific DNA methylations of cytosines in neuronal DNA encode memories in a stable biochemical form. This review describes recent research that elucidates the molecular mechanisms used by the mammalian brain to form DNA methylcytosine encoded memories. For example, neuron activation initiates cytosine demethylation by stimulating DNA topoisomerase II beta (TOP2B) protein to make a temporary DNA double-strand break (repaired within about 2 hours) at a promoter of an immediate early gene, EGR1, allowing expression of this gene. The EGR1 proteins then recruit methylcytosine dioxygenase TET1 proteins to initiate demethylation at several hundred genes, facilitating expression of those genes. Initiation of demethylation of cytosine also occurs when OGG1 localizes at oxidized guanine in a methylated CpG site and recruits TET1 for initiation of demethylation at that site. DNMT3A2 is another immediate early gene upregulated by synaptic activity. DNMT3A2 protein catalyzes de novo DNA methylations. These several mechanisms convert external experiences into DNA methylations and initiated demethylations of neuronal DNA cytosines, causing changes in gene expression that are the basis of long-term memories.

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Lu, Qianjin, Donna Ray, David Gutsch, and Bruce Richardson. "Effect of DNA methylation and chromatin structure onITGAL expression." Blood 99, no. 12 (June 15, 2002): 4503–8. http://dx.doi.org/10.1182/blood.v99.12.4503.

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LFA-1 (CD11a/CD18, αLβ2) is an integrin expressed in a tissue-specific fashion and is important in inflammatory and immune responses. Promoter analysis has identified transcription factors that may be involved in CD11a expression, but the mechanisms contributing to its tissue-specific expression are incompletely characterized. In this report we have asked if DNA methylation and/or chromatin structure could contribute to tissue-specific CD11a expression. Bisulfite sequencing was used to compare methylation patterns in the promoter and 5′ flanking regions of the ITGAL gene, encoding CD11a, in normal human T cells, which express LFA-1, and fibroblasts, which do not. The region was found to be heavily methylated in fibroblasts but not T cells, and methylation correlated with an inactive chromatin configuration as analyzed by deoxyribonuclease 1 sensitivity. Patch methylation of the promoter region revealed that promoter activity was methylation-sensitive but that methylation of the 5′ flanking regions more than 500 base pairs 5′ to the transcription start site could also suppress promoter function. Treating fibroblasts with a DNA methylation inhibitor decreased ITGAL promoter methylation and increased CD11a messenger RNA. The results thus indicate that methylation and chromatin structure may contribute to the tissue-specific expression of CD11a.

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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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McClelland, M., and M. Nelson. "Effect of site-specific methylation on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 20, suppl (May 11, 1992): 2145–57. http://dx.doi.org/10.1093/nar/20.suppl.2145.

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Nelson, Michael, Eberhard Raschke, and Michael McClelland. "Effect of site-specific methylation on restriction endonucleases and DNA modification methyltransferases." Nucleic Acids Research 21, no. 13 (1993): 3139–54. http://dx.doi.org/10.1093/nar/21.13.3139.

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Narasimhan, Supraja, Virginia R. Falkenberg, Maung M. Khin, and Mangalathu S. Rajeevan. "Determination of quantitative and site-specific DNA methylation of perforin by pyrosequencing." BMC Research Notes 2, no. 1 (2009): 104. http://dx.doi.org/10.1186/1756-0500-2-104.

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Wen, Hui, Hui Wang, Honghong Wang, Jingli Yan, Hui Tian, and Zhengping Li. "Ultrasensitive detection of site-specific DNA methylation by loop-mediated isothermal amplification." Anal. Methods 8, no. 27 (2016): 5372–77. http://dx.doi.org/10.1039/c6ay00999a.

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30

Nelson, M., and M. McClelland. "Effect of site-specific methylation on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 17, suppl (January 1, 1989): r389—r415. http://dx.doi.org/10.1093/nar/17.suppl.r389.

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Kishton, Rigel J., Sean E. Miller, Heather Perry, Tera Lynch, Mayur Patel, Vinayak K. Gore, Giridhar R. Akkaraju, and Sridhar Varadarajan. "DNA site-specific N3-adenine methylation targeted to estrogen receptor-positive cells." Bioorganic & Medicinal Chemistry 19, no. 17 (September 2011): 5093–102. http://dx.doi.org/10.1016/j.bmc.2011.07.026.

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Gaido, M. L., and J. S. Strobl. "Inhibition of rat growth hormone promoter activity by site-specific DNA methylation." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1008, no. 2 (July 1989): 234–42. http://dx.doi.org/10.1016/0167-4781(80)90014-7.

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Genereux, D. P., B. E. Miner, C. T. Bergstrom, and C. D. Laird. "A population-epigenetic model to infer site-specific methylation rates from double-stranded DNA methylation patterns." Proceedings of the National Academy of Sciences 102, no. 16 (April 12, 2005): 5802–7. http://dx.doi.org/10.1073/pnas.0502036102.

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Caspers, Maarten, Sara Blocquiaux, Ruben Charlier, Sara Knaeps, Johan Lefevre, Katrien De Bock, and Martine Thomis. "Intensity-Specific Differential Leukocyte DNA Methylation in Physical (In)Activity: An Exploratory Approach." Twin Research and Human Genetics 21, no. 2 (March 27, 2018): 101–11. http://dx.doi.org/10.1017/thg.2018.10.

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The aim of this exploratory study was to investigate how sedentary behavior (SB) and physical activity (PA) influence DNA methylation at a global, gene-specific, and health-related pathway level. SB, light PA (LPA), and moderate-to-vigorous PA (MVPA) were assessed objectively for 41 Flemish men using the SenseWear Pro 3 Armband. CpG site-specific methylation in leukocytes was determined using the Illumina HumanMethylation 450 BeadChip. Correlations were calculated between time spent on the three PA intensity levels and global DNA methylation, using a z-score-based method to determine global DNA methylation levels. To determine whether CpG site-specific methylation can be predicted by these three PA intensity levels, linear regression analyses were performed. Based on the significantly associated CpG sites at α = 0.005, lists were created including all genes with a promoter region overlapping these CpG sites. A biological pathway analysis determined to what extent these genes are overrepresented within several pathways. No significant associations were observed between global DNA methylation and SB (r = 0.084), LPA (r = -0.168), or MVPA (r = -0.125), although the direction of the correlation coefficients is opposite to what is generally reported in literature. SB has a different impact on global and gene-specific methylation than PA, but also LPA and MVPA affect separate genes and pathways. Furthermore, the function of a pathway seems to determine its association with SB, LPA, or MVPA. Multiple PA intensity levels, including SB, should be taken into account in future studies investigating the effect of physical (in)activity on human health through epigenetic mechanisms.

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van der Woude, Marjan, W. Bradley Hale, and David A. Low. "Formation of DNA Methylation Patterns: Nonmethylated GATC Sequences in gut and papOperons." Journal of Bacteriology 180, no. 22 (November 15, 1998): 5913–20. http://dx.doi.org/10.1128/jb.180.22.5913-5920.1998.

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ABSTRACT Most of the adenine residues in GATC sequences in theEscherichia coli chromosome are methylated by the enzyme deoxyadenosine methyltransferase (Dam). However, at least 20 GATC sequences remain nonmethylated throughout the cell cycle. Here we examined how the DNA methylation patterns of GATC sequences within the regulatory regions of the pyelonephritis-associated pilus (pap) operon and the glucitol utilization (gut) operon were formed. The results obtained with an in vitro methylation protection assay showed that the addition of the leucine-responsive regulatory protein (Lrp) to pap DNA was sufficient to protect the two GATC sequences in the pap regulatory region, GATC-I and GATC-II, from methylation by Dam. This finding was consistent with previously published data showing that Lrp was essential for methylation protection of these DNA sites in vivo. Methylation protection also occurred at a GATC site (GATC-44.5) centered 44.5 bp upstream of the transcription start site of thegutABD operon. Two proteins, GutR and the catabolite gene activator protein (CAP), bound to DNA sites overlapping the GATC-44.5-containing region of the gutABD operon. GutR, an operon-specific repressor, was essential for methylation protection in vivo, and binding of GutR protected GATC-44.5 from methylation in vitro. In contrast, binding of CAP at a site overlapping GATC-44.5 did not protect this site from methylation. Mutational analyses indicated that gutABD gene regulation was not controlled by methylation of GATC-44.5, in contrast to regulation of Pap pilus expression, which is directly controlled by methylation of thepap GATC-I and GATC-II sites.

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Małodobra-Mazur, Małgorzata, Aneta Cierzniak, Krzysztof Kaliszewski, and Tadeusz Dobosz. "PPARG Hypermethylation as the First Epigenetic Modification in Newly Onset Insulin Resistance in Human Adipocytes." Genes 12, no. 6 (June 9, 2021): 889. http://dx.doi.org/10.3390/genes12060889.

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Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose uptake. Epigenetic modifications associated with obesity and IR are some of the main mechanisms leading to IR pathogenesis. The mesenchymal stem cells of adipose tissue (subcutaneous (SAT) and visceral (VAT)) were collected during abdominal surgery. IR was induced ex vivo by palmitic acid. DNA methylation was determined at a global and site-specific level. We found higher global DNA methylation in IR adipocytes after 72 h following IR induction. Furthermore, numerous genes regulating insulin action (PPARG, SLC2A4, ADIPOQ) were hypermethylated in IR adipocytes; the earliest changes in site-specific DNA methylation have been detected for PPARG. Epigenetic changes appear to be mediated through DNMT1. DNA methylation is an important component of IR pathogenesis; the PPARG and its epigenetic modification appear to be the very first epigenetic modification in newly onset IR and are probably of the greatest importance.

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Mullins, L. J., G. Veres, C. T. Caskey, and V. Chapman. "Differential methylation of the ornithine carbamoyl transferase gene on active and inactive mouse X chromosomes." Molecular and Cellular Biology 7, no. 11 (November 1987): 3916–22. http://dx.doi.org/10.1128/mcb.7.11.3916-3922.1987.

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Ornithine carbamoyl transferase (Oct) is an X-linked gene which exhibits tissue-specific expression. To determine whether methylation of specific CpG sequences plays a role in dosage compensation or tissue-specific expression of the gene, 13 potentially methylatable sites were identified over a 30-kilobase (kb) region spanning from approximately 15 kb upstream to beyond exon II. Fragments of the Mus hortulanus Oct gene were used as probes to establish the degree of methylation at each site. By considering the methylation status in liver (expressing tissue) versus kidney (nonexpressing tissue) from male and female mice, the active and inactive genes could be investigated on active and inactive X-chromosome backgrounds. One MspI site, 12 kb 5' of the Oct-coding region, was cleaved by HpaII in liver DNA from males but not in kidney DNA from males and thus exhibited complete correlation with tissue-specific expression of the gene. Six other sites showed partial methylation, reflecting incomplete correlation with tissue-specific expression.

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Mullins, L. J., G. Veres, C. T. Caskey, and V. Chapman. "Differential methylation of the ornithine carbamoyl transferase gene on active and inactive mouse X chromosomes." Molecular and Cellular Biology 7, no. 11 (November 1987): 3916–22. http://dx.doi.org/10.1128/mcb.7.11.3916.

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Ornithine carbamoyl transferase (Oct) is an X-linked gene which exhibits tissue-specific expression. To determine whether methylation of specific CpG sequences plays a role in dosage compensation or tissue-specific expression of the gene, 13 potentially methylatable sites were identified over a 30-kilobase (kb) region spanning from approximately 15 kb upstream to beyond exon II. Fragments of the Mus hortulanus Oct gene were used as probes to establish the degree of methylation at each site. By considering the methylation status in liver (expressing tissue) versus kidney (nonexpressing tissue) from male and female mice, the active and inactive genes could be investigated on active and inactive X-chromosome backgrounds. One MspI site, 12 kb 5' of the Oct-coding region, was cleaved by HpaII in liver DNA from males but not in kidney DNA from males and thus exhibited complete correlation with tissue-specific expression of the gene. Six other sites showed partial methylation, reflecting incomplete correlation with tissue-specific expression.

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Lavender, P., A. J. L. Clark, G. M. Besser, and L. H. Rees. "Variable methylation of the 5′-flanking DNA of the human pro-opiomelanocortin gene." Journal of Molecular Endocrinology 6, no. 1 (February 1991): 53–61. http://dx.doi.org/10.1677/jme.0.0060053.

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ABSTRACT The pro-opiomelanocortin gene is widely expressed in human tissues, although both transcriptional initiation sites and regulation appear to be tissue specific. In order to determine how promoter and enhancer choice is effected, we have studied the methylation pattern of the gene in a number of normal tissues, tumours and cell lines. Variability of this pattern was observed in the 5′-flanking DNA, particularly at the HpaII site located at −304 bp upstream from the pituitary CAP site. This site was generally methylated in tissues likely to express the predominant extrapituitary (800 nucleotide) message, while in tissues known to express the normal pituitary (1150 nucleotide) message and longer species, a tendency towards undermethylation was observed. Although the sites at which variable methylation occurs did not correspond to established binding sites for regulatory proteins, many of these regions remain to be determined and thus it is possible that methylation may be influential in the tissue-specific regulation of this gene.

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Ling, Li, Meng Ren, Chuan Yang, Guojuan Lao, Lihong Chen, Hengcong Luo, Zhimei Feng, and Li Yan. "Role of site-specific DNA demethylation in TNFα-induced MMP9 expression in keratinocytes." Journal of Molecular Endocrinology 50, no. 3 (February 15, 2013): 279–90. http://dx.doi.org/10.1530/jme-12-0172.

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Inappropriately high expression of matrix metalloproteinase 9 (MMP9) in the late stage of diabetic foot ulcers suppresses wound healing. The underlying mechanisms are not completely understood. Site-specific demethylation was reported to function in the regulation of genes, causing persistent high expression of target genes. Therefore, this study was designed to determine whether site-specific DNA demethylation was a key regulatory component ofMMP9expression in diabetic wound healing, and to further verify the crucial CpG site(s). Human keratinocyte cell line (HaCaT) cells were exposed to tumor necrosis factor a (TNFα), and changes inMMP9expression and DNA methylation status were detected. We found TNFα treatment increased endogenousMMP9expression in HaCaT cells and decreased the DNA methylation percentage at the −36 bp promoter site in a time-dependent manner. Bisulfite sequencing PCR revealed differentially demethylated CpG sites in the human MMP9 promoter region, but only the change at the −36 bp site was statistically significant. Dual-luciferase reporter assays showed that the promoter with only the −36 bp site demethylated had slightly higher transcriptional activity than the promoter with all other sites except the −36 bp site demethylated. Our results demonstrate that site-specific DNA demethylation plays an important role inMMP9expression in TNFα-stimulated keratinocytes. The −36 bp site in theMMP9gene promoter is crucial to this effect, but other CpG sites may exert synergistic effects. Collectively, these data may contribute to the future development of novel therapeutic strategies to treat diabetic foot ulcers and prevent gangrene and amputation.

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Li, Shufen, Zhongju Wang, Lin Zhou, Fu Luo, and Cunyou Zhao. "Fluorescence polarization-based method with bisulfite conversion-specific one-label extension for quantification of single CpG dinucleotide methylation." Genome 58, no. 7 (July 2015): 357–63. http://dx.doi.org/10.1139/gen-2014-0185.

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To quantify the methylation at individual CpG dinucleotide sites in large biological or clinical samples, we developed a bisulfite conversion-specific one-label extension (BS-OLE) method using visualization by fluorescence polarization (FP) measurement of methylation at single CpG sites in small amounts of genomic DNA. Genomic DNA was treated with sodium bisulfite to convert unmethylated cytosine to uracil leaving 5-methylcytosine unaltered, and BS-PCR was used to generate DNA template containing target CpG sites. BS-OLE uses a BS-primer hybridized immediately upstream of the target CpG site being examined and then fluorescent dCTP or dUTP is incorporated into the methylated (CpG) or unmethylated (TpG) form of the target site through single-nucleotide chain extension, yielding an FP ratio between the fluorescent dCTP- and dUTP-incorporated products as a measure of methylation. This provides stable estimates of the methylation level of human genomic DNA and of a 250-bp plasmid DNA segment containing a single TCGA TaqI cleavage site, in accordance with the results of a combined bisulfite restriction analysis method. We used BS-OLE to measure dose-dependent DNA hypomethylation in human embryonic kidney 293T cells treated with the DNA methyltransferase inhibitor 5-aza-dC. BS-OLE is well suited to high-throughput multi-sample applications in biological and medical studies.

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Umezawa, A., H. Yamamoto, K. Rhodes, M. J. Klemsz, R. A. Maki, and R. G. Oshima. "Methylation of an ETS site in the intron enhancer of the keratin 18 gene participates in tissue-specific repression." Molecular and Cellular Biology 17, no. 9 (September 1997): 4885–94. http://dx.doi.org/10.1128/mcb.17.9.4885.

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The activities of ETS transcription factors are modulated by posttranscriptional modifications and cooperation with other proteins. Another factor which could alter the regulation of genes by ETS transcription factors is DNA methylation of their cognate binding sites. The optimal activity of the keratin 18 (K18) gene is dependent upon an ETS binding site within an enhancer region located in the first intron. The methylation of the ETS binding site was correlated with the repression of the K18 gene in normal human tissues and in K18 transgenic mouse tissues. Neither recombinant ETS2 nor endogenous spleen ETS binding activities bound the methylated site effectively. Increased expression of the K18 gene in spleens of transgenic mice by use of an alternative, cryptic promoter 700 bp upstream of the enhancer resulted in modestly decreased methylation of the K18 ETS site and increased RNA expression. Expression in transgenic mice of a mutant K18 gene, which was still capable of activation by ETS factors but was no longer a substrate for DNA methylation of the ETS site, was fivefold higher in spleen and heart. However, expression in other organs such as liver and intestine was similar to that of the wild-type gene. This result suggests that DNA methylation of the K18 ETS site may be functionally important in the tissue-specific repression of the K18 gene. Epigenetic modification of the binding sites for some ETS transcription factors may result in a refractory transcriptional response even in the presence of necessary trans-acting activities.

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Spainhour, John CG, Hong Seo Lim, Soojin V. Yi, and Peng Qiu. "Correlation Patterns Between DNA Methylation and Gene Expression in The Cancer Genome Atlas." Cancer Informatics 18 (January 2019): 117693511982877. http://dx.doi.org/10.1177/1176935119828776.

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Background: DNA methylation is a form of epigenetic modification that has been shown to play a significant role in gene regulation. In cancer, DNA methylation plays an important role by regulating the expression of oncogenes. The role of DNA methylation in the onset and progression of various cancer types is now being elucidated as more large-scale data become available. The Cancer Genome Atlas (TCGA) provides a wealth of information for the analysis of various molecular aspects of cancer genetics. Gene expression data and DNA methylation data from TCGA have been used for a variety of studies. A traditional understanding of the effects of DNA methylation on gene expression has linked methylation of CpG sites in the gene promoter region with the decrease in gene expression. Recent studies have begun to expand this traditional role of DNA methylation. Results: Here we present a pan-cancer analysis of correlation patterns between CpG methylation and gene expression. Using matching patient data from TCGA, 33 cancer-specific correlations were calculated for each CpG site and the expression level of its corresponding gene. These correlations were used to identify patterns on a per-site basis as well as patterns of methylation across the gene body. Using these identified patterns, we found genes that contain conflicting methylation signals beyond the commonly accepted association between the promoter region methylation and silencing of gene expression. Beyond gene body methylation in whole, we examined individual CpG sites and show that, even in the same gene body, some sites can have a contradictory effect on gene expression in cancers. Conclusions: We observed that within promoter regions there was a substantial amount of positive correlation between methylation and gene expression, which contradicts the commonly accepted association. We observed that the correlation between CpG methylation and gene expression does not exhibit in a tissue-specific manner, suggesting that the effects of methylation on gene expression are largely tissue independent. The analysis of correlation associated with the location of the CpG site in the gene body has led to the identification of several different methylation patterns that affect gene expression, and several examples of methylation activating gene expression were observed. Distinctly opposing or conflicting effects were seen in close proximity on the gene body, where negative and positive correlations were seen at the neighboring CpG sites.

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Dukatz, Michael, Sabrina Adam, Mahamaya Biswal, Jikui Song, Pavel Bashtrykov, and Albert Jeltsch. "Complex DNA sequence readout mechanisms of the DNMT3B DNA methyltransferase." Nucleic Acids Research 48, no. 20 (October 26, 2020): 11495–509. http://dx.doi.org/10.1093/nar/gkaa938.

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Abstract DNA methyltransferases interact with their CpG target sites in the context of variable flanking sequences. We investigated DNA methylation by the human DNMT3B catalytic domain using substrate pools containing CpX target sites in randomized flanking context and identified combined effects of CpG recognition and flanking sequence interaction together with complex contact networks involved in balancing the interaction with different flanking sites. DNA methylation rates were more affected by flanking sequences at non-CpG than at CpG sites. We show that T775 has an essential dynamic role in the catalytic mechanism of DNMT3B. Moreover, we identify six amino acid residues in the DNA-binding interface of DNMT3B (N652, N656, N658, K777, N779, and R823), which are involved in the equalization of methylation rates of CpG sites in favored and disfavored sequence contexts by forming compensatory interactions to the flanking residues including a CpG specific contact to an A at the +1 flanking site. Non-CpG flanking preferences of DNMT3B are highly correlated with non-CpG methylation patterns in human cells. Comparison of the flanking sequence preferences of human and mouse DNMT3B revealed subtle differences suggesting a co-evolution of flanking sequence preferences and cellular DNMT targets.

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Xu, Jian-Hong, Ruixian Wang, Xinxin Li, Mihai Miclaus, and Joachim Messing. "Locus- and Site-Specific DNA Methylation of 19 kDa Zein Genes in Maize." PLOS ONE 11, no. 1 (January 7, 2016): e0146416. http://dx.doi.org/10.1371/journal.pone.0146416.

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Suzuki, M., T. Yamada, F. Kihara-Negishi, T. Sakurai, E. Hara, D. G. Tenen, N. Hozumi, and T. Oikawa. "Site-specific DNA methylation by a complex of PU.1 and Dnmt3a/b." Oncogene 25, no. 17 (December 5, 2005): 2477–88. http://dx.doi.org/10.1038/sj.onc.1209272.

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McClelland, Michael, and Michael Nelson. "The effect of site-specific DNA methylation on restriction endonucleases and DNA modification methyltransferases — a review." Gene 74, no. 1 (December 1988): 291–304. http://dx.doi.org/10.1016/0378-1119(88)90305-8.

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Peshavaria, M., and I. N. M. Day. "Methylation patterns in the human muscle-specific enolase gene (ENO3)." Biochemical Journal 292, no. 3 (June 15, 1993): 701–4. http://dx.doi.org/10.1042/bj2920701.

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The methylation status in the human-muscle enolase gene (ENO3) was assayed. Previous sequence data and MspI cleavage sites indicate the presence of a 5′ CpG-rich island of at least 4 kb: none of 22 characterized MspI CCGG sites is methylated in any of muscle, sperm or brain DNA. However a complex pattern of complete and partial methylation of MspI sites that is different between tissues is observed within the ENO3 gene: events at one site may be specific to muscle DNA. The absence of methylation in the promoter region of the ENO3 gene makes it unlikely that methylation plays a causal role either in transcriptional events or in the divergence of enolase-isogene regulation. The role of tissue-specific methylation events within ENO3 remains to be determined.

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Xie, Xuemei, Hongjie Gao, Wanjiang Zeng, Suhua Chen, Ling Feng, Dongrui Deng, Fu-yuan Qiao, et al. "Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level." Clinical Science 129, no. 4 (May 27, 2015): 385–94. http://dx.doi.org/10.1042/cs20140688.

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Among all the participants, the maternal gestational glucose level was positively correlated with placental DNA methylation. The correlation between gestational 2-h post-OGTT glycaemia and CpG site-specific methylation in placenta was stronger in the gestational diabetes group.

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Patil, Vibha, Cyrille Cuenin, Felicia Chung, Jesus R. Rodriguez Aguilera, Nora Fernandez-Jimenez, Irati Romero-Garmendia, Jose Ramon Bilbao, Vincent Cahais, Joseph Rothwell, and Zdenko Herceg. "Human mitochondrial DNA is extensively methylated in a non-CpG context." Nucleic Acids Research 47, no. 19 (September 6, 2019): 10072–85. http://dx.doi.org/10.1093/nar/gkz762.

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Abstract Mitochondrial dysfunction plays critical roles in cancer development and related therapeutic response; however, exact molecular mechanisms remain unclear. Recently, alongside the discovery of mitochondrial-specific DNA methyltransferases, global and site-specific methylation of the mitochondrial genome has been described. Investigation of any functional consequences however remains unclear and debated due to insufficient evidence of the quantitative degree and frequency of mitochondrial DNA (mtDNA) methylation. This study uses WGBS to provide the first quantitative report of mtDNA methylation at single base pair resolution. The data show that mitochondrial genomes are extensively methylated predominantly at non-CpG sites. Importantly, these methylation patterns display notable differences between normal and cancer cells. Furthermore, knockdown of DNA methyltransferase enzymes resulted in a marked global reduction of mtDNA methylation levels, indicating these enzymes may be associated with the establishment and/or maintenance of mtDNA methylation. DNMT3B knockdown cells displayed a comparatively pronounced global reduction in mtDNA methylation with concomitant increases in gene expression, suggesting a potential functional link between methylation and gene expression. Together these results demonstrate reproducible, non-random methylation patterns of mtDNA and challenge the notion that mtDNA is lowly methylated. This study discusses key differences in methodology that suggest future investigations must allow for techniques that assess both CpG and non-CpG methylation.

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