Microarrays and DNA methylation profiling
Dr.
Axel Schumacher © 2004-2007
The method described in detail
below is based on the analysis of the enriched unmethylated DNA fraction, using
a series of treatments with methylation-sensitive restriction enzymes, adaptor
ligation, PCR amplification, and quantitative mapping of unmethylated DNA
sequences using microarrays. The key advantages of this approach are the
ability to investigate DNA methylation patterns using very small DNA amounts
and also relatively high informativeness in comparison to the other restriction
enzyme- based strategies for DNA methylation profiling (1).
1. Introduction

Fig 1: Schematic outline of the microarray-based method for identification of
DNA methylation differences in genomic DNA. Samples are cleaved by
methylation-sensitive restriction endonucleases, such as HpaII and Hin6I,
ligated to the CpG-overhang specific adapter, and then cut by McrBC to
eliminate residual methylated DNA fragments. The resulting unmethylated DNA
fragments are then selectively enriched by adapter-specific aminoallyl-PCR,
labelled, and hybridized to microarrays.
2. Materials
2.1 Adapter design
2.2
Methylation-sensitive cleavage of DNA
1.
Restriction
enzymes: 10 U/µl HpaII (
2.
Spike DNA (optional; see Methods)
2.3 Ligation
2.4 McrBC digestion
2.5 CpG-specific adapter amplification
2.6 Purification of amplification product
2.7 Labelling
2.9 Hybridization
3.
Methods
Here we present a complete
protocol of DNA methylation profiling using the unmethylated fraction of the
genome. This protocol works with most microarray types, as exemplified here
with CpG island- and oligonucleotide microarrays. A detailed description of how
specific ‘epigenetic’ microarrays are designed and how the slides are processed
can be found in Schumacher et al., 2006 (1). DNA samples can either be
interrogated as pairs (tester and control) on one array, as described in this
protocol, or hybridized independently with only one fluorescent dye (e.g. for
Affymetrix tiling arrays).
3.1 Adapter design
In the CpG-specific adapter design, the following aspects must be taken
into account:

Fig. 2: Preparation of the
CpG-specific adapter. a:
CG1-adapter components. b: Annealing of the CG-primers produces
a double-stranded adapter that can be identified by electrophoresis as a strong
band (200 pmol loaded; 2.5 % agarose gel).
3.1.1 Adapter preparation
1.
Dissolve the non-phosphorylated
ssDNA oligonucleotides in ST buffer with a
concentration of approximately 800 pmol. The presence of some salt is necessary
for the oligos to hybridize into a double stranded (ds)-adapter. Keep some of the CG-1b oligo, as it will be
later used as a primer to amplify the unmethylated DNA fraction. Measurethe concentration in a spectrophotometer and adjust
the concentration to 400 pmol. (Note: Quantify in
spectrophotometer. Re member the OD260 = 1 of single stranded DNA is equivalent
to 33 µg/ml not 50 µg/ml! This relationship, however, can be inaccurate for
short fragments of DNA, such as oligonucleotides. Base composition and even
linear sequence will affect optical absorbance, hence
the precise value of the OD to mass relationship is unique for each oligo. For
example, 1.0 OD260 of CCCCCCCCCCCC (homopolymeric deoxycytidine) equals 39 micrograms while 1.0 OD260 of
AAAAAAAAAAAA (homopolymeric deoxyadenosine)
equals only 20 micrograms. Do not believe the amount of primer as indicated by
the manufacqturer. Perform the appropriate
calculation (800 pmol primer = 0.0008 x MW of oligo)).
3.2 Methylation-sensitive
cleavage of DNA
Over 260 different methylation-sensitive restriction
enzymes (MSRE’s; incl. isoschizomers)
are now available, however, not all enzymes are useful
and informative for DNA methylation profiling. Informative MSREs
are defined by the number of cleavage fragments that can be ligated to adapters
and efficiently amplified, and are not lost during column-purification steps (3). Some enzymes, although they cut frequently in the genome, produce
fewer informative fragments compared to enzymes which do not cut as frequently.
For example, the non-palindromic AciI (5’-CCGC-3’) recognizes more than twice as many CpG
sites in CpG island regions when compared to HpaII, but on the other hand, produces fewer fragments in the
size-range that can be detected by PCR or amplified fragment
length polymorphism (AFLP) methods (Table 1).
|
MSRE |
Cut site 5’-3’ |
~% of CpGs in CpG islands* |
~% of CpGs in non-CpG islands* |
Fragments/kb in CpG islands* |
Fragments/kb in non-CpG islands* |
|
AciI (SsiI) |
CCGC,
GCGG |
30.60 |
17.36 |
3.23 |
1.79 |
|
Hin6IΔ
(HinP1I) |
GCGC |
14.40 |
5.05 |
3.98 |
0.61 |
|
HpaII
(BsiSI) |
CCGG |
11.70 |
9.33 |
3.98 |
1.18 |
|
Hin1I (BsaHI) |
GRCGYC |
2.6 |
0.9 |
1.92 |
0.11 |
|
HpyCH4IV
(TaiI) |
ACGT |
1.66 |
6.73 |
1.24 |
0.97 |
|
Bsp119I
(AsuII) |
TTCGAA |
0.11 |
0.13 |
0.11 |
<0.02 |
|
Bsu15I
(ClaII) |
ATCGAT |
<0.05 |
0.39 |
<0.02 |
0.02 |
Different requirements for the enzyme reduces
the list of potentially useful and informative MSRE’s
to about 17, which would cover up to 85% of all CpG island CpG dinucleotides,
but less than 50% of all CpG dinucleotides in other genomic regions (3). Here, we demonstrate the
technology with a double-digestion using HpaII and Hin6I enzymes (Note: To gain the most out of restriction
analyses, it is crucial to choose the right enzyme combination for the targets
to be interrogated. For example, some MSRE’s cut
relative frequently in CpG islands, but rarely recognize a sequence outside of
a CpG island region, as is the case for Hin6I (5’-GCGC-3’) or Bsp143II
(5’-PuGCGCPy-3’). In contrast, enzymes such as HpyCH4IV (5’-ACGT-3’) cut
predominantly outside of CpG island sequences and are less useful in the
interrogation of CpG islands, for instance in CpG island-microarray based
studies (3). Several other methods rely on the
specific methylation-sensitive cleavage of the rare cutter NotI
(5’-GCGGCCGC-3’), for example RLGS and AFLP methods and a couple of microarray
approaches (6, 7). However, NotI-sites
are not well represented in the genome and will only provide a very rough overview
of methylation patterns. Hence, it is not advisable to include NotI in genome-wide analyses of e.g. complex diseases).
Before the test DNA can be processed, it is
advantageous to add “spiking” DNA to the gDNA samples. The spiking DNA consists
of ‘alien’ (exogenous) DNA, which allows monitoring of each step of the
experiment (Note:
Additionally, spike DNA can be used to test the methylation-sensitive cleavage
reaction, ligation efficiency, McrBC digestion and PCR reaction. Spiking DNA is
added to the reactions with concentrations equivalent to the template
concentration (1 genome equivalent, GE, assuming 3x109 bp
in the human genome). For example, 16.2 pg of λ plasmid is added to 1 µg of template
DNA. Make 12x GE stock solutions in 1 mM EDTA; aliquot into small volumes and
store at -20°C. To prepare a McrBC digestion control, digest pUC57 with HpaII,
ligate the CG-adapter and premethylate with SssI methylase. McrBC controls are
added to the McrBC cleavage step as premethylated plasmid. Other suitable controls
are ФX174
to test for PCR bias or pBR322 to test the ligation efficiency (1). ФX174 DNA has to be digested separately
with HpaII/Hin6I and then ligated to the CG-adapter. Complementary spiking
oligonucleotides have to be representative sequences of HpaII and Hin6I
cleavage fragments).
As with any microarray experiment, controls are crucial for monitoring experimental variability. Suitable spiking DNA consists of sequences that are frequently spotted on commercially available microarrays, such as Arabidopsis, RNA spikes or artificial sequences. (Note: SNPs within the recognition sites for HpaII and Hin6I may simulate epigenetic differences (8). In order to exclude the impact of DNA sequence variation it is suggested to check the available SNP databases and identify the DNA sequence variation within the restriction sites of the used enzymes. From CpG island microarray studies, the estimate is that 10 to 30% of methylation variation detected in between individuals could, in fact, be due to DNA sequence variation (1). For comparison, in a study for the Human Epigenome Project (HEP), interrogation of 3,273 unique CpG sites on chromosome 6 revealed that 101 CpGs overlapped with known SNPs (3 %) (9). Another way to differentiate DNA sequence effects from genuine epigenetic differences consists of performing an identical microarray experiment on the same DNA sample that has been stripped of all methylated cytosines