期刊
AMERICAN JOURNAL OF HUMAN GENETICS
卷 94, 期 4, 页码 485-495出版社
CELL PRESS
DOI: 10.1016/j.ajhg.2014.02.011
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资金
- National Institutes of Health (NIH) [HG003233, AG042187]
- Swedish AFA Insurance grants
- Swedish Strategic Research Foundation
- European Research Council
- Intramural Research Program of the NIH National Institute on Aging
- MedStar Research Institute
Epigenetic marks such as DNA methylation have generated great interest in the study of human disease. However, studies of DNA methylation have not established population-epigenetics principles to guide design, efficient statistics, or interpretation. Here, we show that the clustering of correlated DNA methylation at CpGs was similar to that of linkage-disequilibrium (LD) correlation in genetic SNP variation but for much shorter distances. Some clustering of methylated CpGs appeared to be genetically driven. Further, a set of correlated methylated CpGs related to a single SNP-based LD block was not always physically contiguous-segments of uncorrelated methylation as long as 300 kb could be interspersed in the cluster. Thus, we denoted these sets of correlated CpGs as GeMes, defined as potentially noncontiguous methylation clusters under the control of one or more methylation quantitative trait loci. This type of correlated methylation structure has implications for both biological functions of DNA methylation and for the design, analysis, and interpretation of epigenome-wide association studies.
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