Table 1 Studies of CpG methylation discordance in monozygotic (MZ) twins
Study | Type | Method | Tissue | MZ pairs, n | Conclusion |
|---|---|---|---|---|---|
Fraga et al. [29] | Cross-sectional, age-stratified | High-performance capillary electrophoresis of total methyl-cytosine content | Peripheral lymphocytes; buccal epithelial cells; muscle biopsy; adipose tissue | 40 | Young MZ twins are nearly identical epigenetically; discordance progresses with age, mediated by a combination of external and/or internal factors· |
Kaminsky et al. [85] | Cross-sectional | Human 12 K CpG island microarrays | White blood cells, buccal epithelial cells, rectal biopsy | 571 | Methylation discordance in MZ twins confirmed;· monochorionic MZ twins significantly more discordant than dichorionic MZ twins.. Epigenetic drift suggested as the main cause of discordance. |
Saffery et al. [86] | Cross-sectional, taken at birth | Bis-seq (IGF2/H19) | Cord blood, mononuclear cells, buccal epithelial cells, placental cells, umbilical vein cells, endothelial cells | 56 | CpG methylation discordance can arise in newborn twins by combination of environmental and/or stochastic factors acting in utero and varies depending on the type of the tissue. |
Wong et al. [87] | Longitudinal, with single 5-year interval | High-throughput mass spectrometry (DRD4, SERT, MAOA) | Buccal cells, epithelial cells | 46 | CpG methylation discordance is present in early childhood and susceptibility to epigenetic change is highly locus-specific.. Environmental influence is the main cause of discordance, with various loci having differential susceptibility to shared and non-shared exposures. |
Talens et al. [88] | Cross-sectional and longitudinal with single 10-year interval | High-throughput mass spectrometry; global methylation and selected loci (IGF2, LEP, CRH, ABCA1, INS, KCNQ1OT1, GNASAS) | Whole blood | 230 | Global and locus-specific methylation increases gradually with age, owing to unique environmental and stochastic factors. |