Additional file 1:

Table S1. Monoallelic methylation levels in individuals.

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Additional file 2:

Fig. S1. Percentage monoallelic methylation for individual 12089 by chromosome. Note that the greater extent to which the × chromosome revealed allele-specific methylation in the Hellman and Chess 2007 experiment was because in that experiment, we were analyzing multiple subclones from each individual in order to define the effects of the × inactivation process on monoallelic methylation.

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Additional file 3:

Table S2. Bisulfite sequencing control experiments.

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Additional file 4:

Table S3. Methylation overlap between different (freshly isolated) tissues of unrelated individuals.

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Additional file 5:

Fig. S2. Monoallelic methylation is largely independent of parental imprinting.

(a, b) Allele-specific methylation that is dependent on the parent of origin is a known feature of parentally imprinted regions. To explore whether parental imprinting is a major contributor to the observed methylation overlap across the genome, we analyzed individuals from three generations. Because the hallmark of an imprinted mark is that the inequality between the two alleles has the same parent of origin (maternal or paternal) in each generation, a sign of imprinting in this experiment would be allele-specifically methylated alleles tending towards having the same parent of origin in the first and the second transmissions observable in three generations. The configurations of the genotypes shown in (a) and (b) are representative of several that can inform such an analysis. (C) Averages and standard deviations for the analyses presented individually in Table S4 (Additional file 6). We observed equal frequencies of the same parent of origin as of a switch in parent of origin. These analyses did not rule out the possibility that a subset of methylation overlap was due to parental imprinting. Indeed, our analyses of the H19/IGF2 differentially methylated region revealed clustering of monoallelically methylated SNPs, suggesting that some methylation overlap could be due to imprinting. However, across the genome, parental imprinting was not a major contributor.

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Additional file 6:

Table S4. Excess of methylation overlap is not due parental imprinting.

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Additional file 7:

Table S5. Sibling pair analyses.

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Additional file 8:

Table S6. Numbers of informative SNPs and of SNPs showing methylation overlap or opposite overlap among fifteen parent-child pairs.

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Additional file 9:

Table S7. Bisulfite sequencing analyses of nearby CpGs. Throughout, the data were consistent with the Affymetrix array data and with what is generally known about CpG methylation across the genome. The analyzed CpGs had a range of distances from the SNP up to 1,045 bp. The predominant pattern is methylation of both alleles, which was found for 26 sites (and three more that were part of a methylation-sensitive restriction enzyme (MSRE) site and therefore we left out of the count). Five sites were methylated on the same allele as the methylated allele reported by the Affymetrix array experiment (and also an additional two sites that were MSREs and again, not counted). Two sites were unmethylated on both alleles. There were no examples of allele-specific methylation on the opposite allele compared with the Affymetrix array experiment.

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