DNA Methylation Guide
Overview, Methods, and Resources

Enabling Epigenetics ResearchDNA Methylation Guide
Overview of DNA Methylation
Since first discovered in bacteria nearly 100 years ago, DNA methylation has been shown to be a crucial epigenetic regulator of gene expression and genomic
organization in nearly all organisms. In eukaryotes, this modification of DNA is found in cytosines (C), where DNA Methyl Transferases (DNMTs) mediate the transfer ofa methyl group to cytosines, converting them to 5-methylcytosine (5-mC). This minor DNA modification can change the activity of DNA without changing the primary
sequence itself.
DNA methylation appears almost exclusively in the context of CpG dinucleotides. Overall, these dinucleotides are relatively rare in the mammalian genome and aremainly clustered in what are called CpG islands, ranging between 500-2,000 base pairs in length. In humans, >60% of these CpG islands are in gene promoters. Whilemost CpG dinucleotides are methylated, those within promoter regions are almost always unmethylated and are associated with transcriptionally active genes. DNA
methylation of promoters is linked with several fundamental processes including genomic imprinting, X-chromosome inactivation, and repression of transposable
elements. Aberrant changes in DNA methylation patterns are associated with many diseases as well as aging.
DNA methylation is reversible. TET enzymes, a family of ten-eleven translocation (TET) methylcytosine dioxygenases are central for DNA demethylation. These enzymes convert 5-mC to 5-hmC. Their further action can catalyze the conversion of 5-hmC to 5-formylctyosine (5-fC) and then to 5-carboxyctyosine (5-caC). Both 5-fC
and 5-caC can then be removed from the DNA sequence by base excision repair and replaced by an unmethylated cytosine. While 5-hmC was originally believed to
be an incidental mark on the way to demethylation, evidence has since shown that the Tet family of proteins and 5-hmC are in fact involved in normal development aswell as many disease states. In mammals, 5-hmC is found in high levels in the brain and in other tissues of the central nervous system.
Many scientists have engaged in studies to understand the distribution of DNA methylation, leading to the emergence of numerous methods for mapping 5-mC and5-hmC. The sheer number of options can be overwhelming and make it difficult to know where to start. However, while there are many approaches for studying DNA
methylation, the best tactic can be determined based on the goals and resources for a particular experiment, with each method having advantages and drawbacks.

NH2

NH2

DNMT3ADNMT3B

N
O

DNMT1

N
H
Cytosine
(C)

NH2

TET2
TET3

N
O

TET1

N
H

5-Methylcytosine(5-mC)

OH

N
O

N
H

5-Hydroxymethylcytosine(5-hmC)i
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What’s Inside
Global Quantification of DNA Methylation

1• Overview• Methods and Comparison• Comparison of Methods• Sample Data and Tools to Study Global Quantification• Products Available to Study Global DNA Methylation Levels

DNA Methylation Enrichment

3• Overview• Methods and Comparison• Comparison of Methods• Sample Data and Tools for DNA Enrichment• Products & Services for Genome-Wide & Gene-Specific Analysis

Single-Nucleotide Resolution Analysis of DNA Methylation

7• Overview• Methods and Comparison• Comparison of Methods• Sample Data and Tools for Single-Nucleotide Analysis• Products & Services for Single-Nucleotide Resolution 5-mc Analysis

Additional Resources

11• Webinars• Podcasts• Blogsii
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Global Quantification of DNA Methylation
Overview
Global measurements of DNA methylation refer to the total level of 5-mC or 5-hmC content relative to the total cytosine content in sample DNA. Variations in overall
genomic DNA methylation levels are observed across different developmental states and tissue types, as well as in various disease states. Research indicates a global
decrease in 5-hmC levels associated with numerous cancers, while changes to the abundance of 5-hmC has been associated with neurodegenerative disorders
making it a proposed molecular biomarker.

Methods and Comparison
Common methods used to measure global DNA methylation levels include chromatographic methods such as HPLC and mass spectrometry. However, while thesemethods are very sensitive and accurate, they require a high level of expertise, are low throughput and time-consuming. Global ELISA-based DNA methylation assays
are a popular alternative method because they are easy to conduct and only require standard lab equipment. For these types of assays, DNA is first immobilized onto
the wells of a 96-well plate. Methylated or hydroxymethylated cytosines in the DNA are then identified using either a 5-mC or a 5-hmC antibody, HRP-conjugatedsecondary antibody, and colorimetric detection reagents. By generating a standard curve using DNA with known methylation, the percentage of 5-mC or 5-hmC canbe determined for each DNA sample. Clinical researchers can use these high-throughput assays when screening large numbers of patient samples from their study
cohorts.

Comparison of Methods
MethodGlobal 5mC/5hmC ELISA

LC-MS/MS

Method Overview

Total DNA or a subsampled surrogate is bound to wells of an ELISA plate. A capture
antibody for 5mC/5hmC binds to methylated DNA. Secondary antibody and developer
are used for colorimetric detection.

Liquid chromatography coupled with mass spectrometry is used on digested DNA.

Input

> 5-10 ng

50-100 ng

Resolution

GenomeGenomeCoverage

Global quantitation of methylation in DNA.

Global quantitation of methylation in DNA.

Advantages

Easy and inexpensive to use. HTP friendly.

Highly sensitive. Works with poor quality DNA (FFPE).

Disadvantages

Does not tell you which regions of the genome have methylation changes.

Requires specialized equipment. Low through-put.

Cost

$

$

Best Application

Useful for screening/monitoring samples for changes in DNA methylation related todisease, aging, or environmental factors like smoking or obesity.

Considered “gold-standard” for global measurements of DNA methylation quantification.

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Sample Data and Tools to Study Global Quantification<25 yo>60 yoGlobal DNA Methylation – LINE-1 Assay shows changes in 5-mC levels in cfDNA with age.
cfDNA was isolated from human serum samples from healthy “normal” adults <25 yo (N=6, mean: 21.83) and >60 yo (N=9, mean:65.89) Following the Global DNA Methylation Line-1 Kit
protocol, without MseI digestion, 25 ng of cfDNA was used per well. The % 5-mC for each sample was calculated as a percentage of detectable CpG residues in the LINE-1 probe region,
using the methylated DNA standards included in the kit. All samples were done in triplicate. Boxplot shows 25%-75% (☐) , min-max (Ι), average (x), and median (-) % 5-mC.

Products Available to Study Global DNA Methylation Levels
Product

FormatCatalog Number

Global DNA Methylation Assay-LINE-1

1 x 96 rxns

55017

Global 5-hmC DNA ELISA Kit

1 x 96 rxns

55025

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DNA Methylation Enrichment
Overview
Enrichment methods for mapping DNA methylation rely on the selective capture of methylated fragments from the rest of the genomic DNA. This is typically accomplished by antibody immunoprecipitation methods or with enzymes such as methyl-CpG binding domain (MBD) proteins or beta-glucosyltransferase which are used to
selectively tag methylated fragments.
While the resolution for methylated (5-mC) and hydroxymethylated (5-hmC) detection is limited due to the size of the DNA fragments captured, typically between 100300 nucleotides, the methods greatly reduce costs as only a small fraction of the DNA requires sequencing. This makes them great screening methods for identifying
differently methylated regions of DNA between samples, especially when there is no prior knowledge of where it might occur. Once differently methylated regions are
determined, methods with higher resolution can be used to focus on just those regions.

Methods and Comparison
MeDIP/hMeDIP
Methylated DNA Immunoprecipitation (MeDIP) and hydroxymethylated DNA Immunoprecipitation (hMeDIP) are antibody immunoprecipitation methods that utilize
methylation specific antibodies to recognize and capture 5-mC and 5-hmC respectively. Antibodies specific for either 5-mC or 5-hmC are used to selectively tag methylated genomic DNA fragments. Antibody tagged fragments are then captured by magnetic beads that bind the FC region of the antibody. The enriched methylated
DNA fragments can then be sequenced.
MeDIP and hMeDIP can capture any methylated cytosines regardless of the sequence context as the antibodies do not require CpGs for binding. However, the antibody
will be biased towards capturing highly methylated regions of DNA as the antibodies generally require more than one methylated cytosine per fragment to bind.
MBD-Seq
MBD-capture or MBD-seq is an enzymatic based method for the enrichment of methylated DNA fragments. Instead of an antibody it uses recombinant methyl-binding
protein MBD2b to selectively bind 5-methylcytosine DNA. Sheared DNA is mixed with His-tagged MBD2b protein so that methylated DNA can then be captured bynickel-coated magnetic beads.
One advantage of the methyl-CpG binding protein enrichment strategy over MeDIP, is the input DNA sample does not require denaturing, as the protein can recognize
methylated DNA in its native double-strand form. Also, the input required for MBD-seq is lower than for MeDIP, making this method ideal for cfDNA and looking forbiomarkers related to diseases like cancer. Note that the MBD2b protein only binds to CpG methylated DNA, making this technique ideal for researchers studying CpG
Islands but it will miss non CpG methylation.
hME-SealhME-Seal uses a beta-glucosyltransferase (βGT) enzyme to transfer an engineered glucose moiety, UDP-Azide-Glucose, onto the hydroxyl group of 5-hmC. A chemicallabeling reaction then attaches a biotin to the glucose so that fragments can be captured by streptavidin beads.

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Because βGT modifies 5-hmC regardless of sequence context, both CpG and non-CpG methylation can be identified. Like MBD-seq, the process works with dsDNA
and works for low input samples. This makes the technique ideal for samples like cfDNA, which are often used when looking for biomarkers related to diseases likecancer.

Comparison of Methods
MethodMeDIP-Seq or hMeDIP-Seq

MBD-Capture/MBD-Seq

5hmC-Seal

Method Overview

Uses a methylation (5mC/5hmC) specific antibody to
perform immunoprecipitation on fragmented DNA.

A tagged methyl-CpG binding domain (MBD) protein isused to capture methylated CpG from fragmented DNA.

Uses beta-Glucosyltransferase to selectively transfer glucose from a UDP-Azide-Glucose donor to 5hmC. A biotin
conjugate is then attached to the modified glucosyl-5-hmC
so that tagged fragments can be captured by streptavidin
beads.

Input>100 ng>5-10 ng

>10 ngResolution

100-500 bp

100-500 bp

100-500 bp

Coverage~88% CpG sites

Up to 27 million CpGs

>300k 5-hmCs

Advantages

Covers both CpG and non CpG sites.

Requires less sample than MeDIP. More sensitive andspecific to CpG than MeDIP.

Requires less sample than hMeDIP. More sensitive andspecific than antibody-based detection of 5hmC.

Disadvantages

MeDIP requires ssDNA. Antibody based techniques
produce higher background than enzymatic based.

Misses non-CpG methylation.

Cost

$$

$$

$$

Best Application

Cost effective method for determining differently
methylated regions of the genome related to disease orenvironmental exposure.

Cost effective method for determining differently
methylated regions of the genome related to disease orenvironmental exposure.

Commonly used to detect changes in hydroxymethylationin cfDNA samples that could be used for biomarkers fordisease.

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Sample Data and Tools for DNA Enrichment

MeDIP-Seq uncovers aging-associated differential methylation patterns in cfDNA.
Serum samples were collected in serum separator tubes (SST) from healthy “normal” adults, two <25 yo and two >60. Cell-Free DNA (cfDNA) was purified and 200 ng cfDNA was for MeDIPseq. MeDIP and Input libraries were sequenced (38bp PE chemistry on Next-Seq500) and processed as per Active Motif’s standard pipeline for MeDIP-Seq. Peaks called using MACS2
relative to input (p-value cutoff = 1.00x10-7).

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hMeDIP-Seq performed on human brain.
hMeDIP was performed with a 5-Hydroxymethylcytosine (5-hmC) antibody (Active Motif Catalog No. 39999) and 2 µg of human brain DNA. Enriched DNA was sequenced on the Illumina
GA II and 19 million sequence tags were mapped to identify regions enriched for 5-hmC. The image above shows an 8 Mb region on chromosome 5 with 5-hmC enrichment across several
gene bodies.

Products & Services for Genome-Wide & Gene-Specific Analysis
Product / Service

FormatCatalog number

MeDIP Kit

10 rxns

55009

hMeDIP Kit

10 rxns

55010

MethylPath MeDIP-Seq Service

Custom-Contact Us

25025

MethylPath hMeDIP-Seq Service

Custom-Contact Us

25052

MethylCollector

30 rxns

55026

1 vial

55020

TM
TM

TM

MBD Capture Kit

UDP-Azide-Glucose

6
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Single-Nucleotide Resolution Analysis of DNA Methylation
Overview
When researchers need to know precisely which cytosine residues are methylated a DNA methylation assay with single-nucleotide resolution is required. Historicallythese methods involve performing bisulfite conversion. Bisulfite Conversion reveals the methylation state of each cytosine in DNA. DNA is first denatured (madesingle-stranded) and then treated with sodium bisulfite. Sodium bisulfite selectively changes unmethylated cytosines into uracils through deamination, while leaving
methylated cytosines (both 5-mC and 5-hmC) unchanged. By then amplifying the treated DNA with PCR, uracils are further converted to thymines. At this point all
nucleotides that were originally unmethylated cytosines become thymines while those that were methylated cytosines remain cytosines. The result is a clear nucleotide
difference between methylated and unmethylated cytosines that can be easily identified by comparison to the original reference genome. A newer alternative to bisulfite conversion is to use enzymes such as TET2 and APOBEC3A to selectively convert cytosines to uracils. This approach avoids the damage that bisulfite conversion
does to DNA but does not change resolution, cost, or coverage between the different techniques below.

Methods and Comparison
Whole Genome Bisulfite Sequencing (WGBS)
Often referred to as the “gold standard” for analysis of DNA methylation, Whole Genome Bisulfite Sequencing (WGBS) provides the greatest coverage and resolutionof any DNA methylation analysis technique. Genomic DNA is first isolated and undergoes bisulfite conversion. The DNA is then adapter ligated and used to preparea sequencing library. Following sequencing, DNA is bioinformatically analyzed to reveal methylated cytosines across the entire genome. The drawback to such comprehensive coverage is the high cost of sequencing and the complex data output. To achieve 15x coverage of the human methylome, a minimum of 800 million reads(100PE) is recommended. Despite the higher cost, WGBS may be preferred in situations where methylation in low CpG density regions is required or when looking at
non-GpG methylation. The study of methylation in stem cells, neurons, and oocytes are some such examples.
Reduced Representation Bisulfite Sequencing (RRBS)
Reduced Representation Bisulfite Sequencing (RRBS) uses restriction enzymes together with DNA size selection to greatly reduce the percentage of the genome thatmust be sequenced. DNA is first digested using methylation-insensitive restriction enzymes (commonly MspI) which generate fragments containing CpG dinucleotides
at the ends. Fragments are then adapter ligated and size selected so that CpG rich regions of DNA small enough to be sequenced remain. Enriched fragments canthen be bisulfite converted and amplified to reveal methylated cytosines and sequenced. RRBS captures 80-85% of CpG islands and 50-60% of human promoters while
sequencing only 3% of the genome. This offers a huge cost savings over WBGS. RRBS is a good method to look for single base resolution changes in CpG rich regions
like promotors which are commonly abnormally methylated in diseases such as cancer. However, it will miss 85-90% of CpGs in the genome.
Targeted Bisulfite Sequencing
Targeted bisulfite sequencing allows for very accurate analysis of methylation at single nucleotide resolution for specific regions of interest. It begins with bisulfite
conversion of DNA and then uses primers to PCR amplify targeted loci. Primers must be designed to cover each region. Amplicons undergo library construction and aresequenced. By limiting sequencing to a small number of multiplexed amplicons, high sequencing depth of cytosines is achieved for those regions at low cost. Targetedbisulfite sequencing is a good method to use when looking at just a hand-full of loci. Much more than this, and the costs will stack up quickly and it’s better to use anassay with more global coverage.

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Methylation Arrays
Methylation arrays allow for quantification of methylation at selected cytosines in multiplexed samples on a chip. DNA is first bisulfite treated and PCR amplified toreveal the methylation pattern of the DNA. The DNA is then combined with complementary probes which target specific methylation sites. Two probes per target can beused, one complimentary to the methylated state and the other to the unmethylated state of the cytosine. Alternatively, a single probe can be used which distinguishes
between methylation states based on a single base extension over the methylation site. Differently tagged nucleotides reveal levels of methylation from a fluorescentsignal that is specific and quantifiable for the unmethylated or methylated state at each site. Methylation arrays are easy to use and reproducible. Coverage is very high(>96) for CpG islands, but they will miss most other (>98%) CpG sites in the genome. They also can only currently be used for human and mouse samples. These are
great for clinical screening of samples for aberrant methylation differences in CpG islands.

Comparison of Methods
MethodWGBS - Whole-Genome Bisulfite
Sequencing

RRBS - Reduced Representation Bisulfite
Sequencing

Targeted Bisulfite Sequencing

Methylation Bead Array

Method Overview

DNA is bisulfite treated and PCR amplified
to reveal the methylation pattern of theDNA. The DNA is then used to prepare asequencing library.

A restriction enzyme, typically MspI, is firstused to cut DNA fragments in regions ofhigh CG, which are common in CpG islands
and promotors. DNA is then size selected
for 40-220 bp fragments, adapter ligated,and bisulfite converted.

DNA is bisulfite treated and PCR amplified
to reveal the methylation pattern of theDNA. PCR primers are then used to amplify
targeted loci. These amplicons undergo
library construction and are sequenced.

DNA is bisulfite treated and PCR amplified
to reveal the methylation pattern of theDNA. It is then combined with DNA probes
which target specific methylation sites.

Input>500 ng>200 ng>1-50 ng

250 ngResolution

Single baseSingle baseSingle baseSingle base

Coverage

28 million CpGs

3-5 million CpGs, 80-85% CpG Islands

Regions of selected amplicons; typically<10.

850,000 CpGs, >96% CpG islands

Advantages

Comprehensive coverage of methylated
and unmethylated regions.

Can sequence regions dense in CpG
methylation genome wide at single-baseresolution for lower cost than WGBS.

Once primers are designed, high sequencing depth at low cost for regions of interest.

Easy, reproducible, works with FFPE
samples

Disadvantages

Expensive & time consuming. Not practicalfor high throughput. Does not distinguish
5mC from 5hmC.

Biased towards regions enriched in CCGG.
Genes which have no or sparse CCGG
motif not covered. Does not distinguish
5mC from 5hmC.

Primers must be designed for every region.
Does not distinguish 5mC from 5hmC.

For human and mouse only. Misses 95% of
CpG sites. Does not distinguish 5mC from
5hmC.

Cost

$$$$

$$$

$$

$$$

Best Application

Ideal when interested in low-CpG-density
regions, intergenic “gene deserts”, orpartially methylated domains and distal
regulatory elements, that would be missed
by RRBS

Profiling CpG islands and promoters

Great when interested in methylation in asmall number (<8) of regions of interest,
especially if not in CpG islands.

Screening of clinical samples for aberrant
methylation in CpG islands.

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Sample Data and Tools for Single-Nucleotide Analysis

RRBS data from human samples.
The displayed regions are representative regions from the genome-wide data set and shows differential DNA methylation at an exon of CD19. Each block is a separate data point with red
representing a methylated cytosine and blue representing an unmethylated base.

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72

1

NormalPatients2

3

Diseased Disease Model
Patients
Cell Line

4

5

6

7

8

9

CpG Site

48

24

1
0

50

100

% DNA Methylation

Heat map of Targeted Next-Gen Bisulfite Sequencing data.
MBD-Seq was first performed on 3 samples of interest to identify differentially methylated regions. One identified region was used for Targeted Next-Gen Bisulfite Sequencing on a broader
population of 9 samples. This heat map shows the single base pair resolution of the 72 CpGs in this region across the 9 samples.

Products & Services for Single-Nucleotide Resolution 5-mc Analysis
Product / Service

FormatCatalog Number

Reduced Representation Bisulfite Sequencing (RRBS)

Custom-Contact Us

25069

Targeted Bisulfite Sequencing Service

Custom-Contact Us

25035

FFPE Bisulfite Conversion Kit

40 rxns

55021

Bisulfite Conversion Kit

50 rxns

55016

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Additional Resources
Webinars• Anchor-Based Bisulfite Sequencing (ABBS) Determines Genome-wide DNA Methylation

Podcasts• CpG Islands, DNA Methylation, and Disease (Sir Adrian Bird)• The Role of DNA Methylation in Epilepsy (Katja Kobow)• DNA Methylation and Mammalian Development (Déborah Bourc’his)• Effects of DNA Methylation on Diabetes (Charlotte Ling)• Effects of DNA Methylation on Chromatin Structure and Transcription (Dirk Schübeler)

Blogs• ABBS – A Novel Method to Map DNA Methylation Genome-Wide at Base Resolution• DNA Methylation in Cell-free DNA (cfDNA): Benefits, Limitations & Future Potential for Precision Medicine• Complete Guide to Using Reduced Representation Bisulfite Sequencing (RRBS) for Genome-Wide DNA Methylation Analysis

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References
Deaton AM, Bird A (2011). “CpG islands and the regulation of transcription”. Genes Dev. 25 (10): 1010–22. doi:10.1101/gad.2037511. PMC 3093116. PMID 21576262. (CGI)
Jeziorska DM, Murray RJS, De Gobbi M, Gaentzsch R, Garrick D, Ayyub H, Chen T, Li E, Telenius J, Lynch M, Graham B, Smith AJH, Lund JN, Hughes JR, Higgs DR,
Tufarelli C. DNA methylation of intragenic CpG islands depends on their transcriptional activity during differentiation and disease. Proc Natl Acad Sci U S A. 2017 Sep
5;114(36):E7526-E7535. doi: 10.1073/pnas.1703087114. Epub 2017 Aug 21. PMID: 28827334; PMCID: PMC5594649. (CGI)
Kurdyukov S, Bullock M. DNA Methylation Analysis: Choosing the Right Method. Biology (Basel). 2016 Jan 6;5(1):3. doi: 10.3390/biology5010003. PMID: 26751487;
PMCID: PMC4810160. (Global Methylation)
Sun Z, Cunningham J, Slager S, Kocher JP. Base resolution methylome profiling: considerations in platform selection, data preprocessing and analysis. Epigenomics.
2015 Aug;7(5):813-28. doi: 10.2217/epi.15.21. Epub 2015 Sep 14. PMID: 26366945; PMCID: PMC4790440. (WBGS/RRBS)
Xiao, Y., Yu, F., Pang, L. et al. MeSiC: A Model-Based Method for Estimating 5 mC Levels at Single-CpG Resolution from MeDIP-seq. Sci Rep 5, 14699 (2015). https://doi.
org/10.1038/srep14699 (MeDIP coverage)
Sun Z, Cunningham J, Slager S, Kocher JP. Base resolution methylome profiling: considerations in platform selection, data preprocessing and analysis. Epigenomics.
2015 Aug;7(5):813-28. doi: 10.2217/epi.15.21. Epub 2015 Sep 14. PMID: 26366945; PMCID: PMC4790440. (RRBS coverage)
Aberg KA, Chan RF, van den Oord EJCG. MBD-seq - realities of a misunderstood method for high-quality methylome-wide association studies. Epigenetics. 2020
Apr;15(4):431-438. doi: 10.1080/15592294.2019.1695339. Epub 2019 Nov 25. PMID: 31739727; PMCID: PMC7153543. (MBD-Seq)
Clark C, Palta P, Joyce CJ, Scott C, Grundberg E, Deloukas P, Palotie A, Coffey AJ. A comparison of the whole genome approach of MeDIP-seq to the targeted approachof the Infinium HumanMethylation450 BeadChip(®) for methylome profiling. PLoS One. 2012;7(11):e50233. doi: 10.1371/journal.pone.0050233. Epub 2012 Nov 29. PMID:
23209683; PMCID: PMC3510246. (Me-DIP)
Beck D, Ben Maamar M, Skinner MK. Genome-wide CpG density and DNA methylation analysis method (MeDIP, RRBS, and WGBS) comparisons. Epigenetics. 2022
May;17(5):518-530. doi: 10.1080/15592294.2021.1924970. Epub 2021 May 11. PMID: 33975521; PMCID: PMC9067529. (MeDIP, RRBS, WGBS)Song CX, Yi C, He C. Mapping recently identified nucleotide variants in the genome and transcriptome. Nat Biotechnol. 2012 Nov;30(11):1107-16. doi: 10.1038/nbt.2398.
PMID: 23138310; PMCID: PMC3537840. (hMeDIP/hmE-Seal)

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