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Random field modeling of multi-trait multi-locus association for detecting methylation quantitative trait loci.

Chen Lyu1,2, Manyan Huang1, Nianjun Liu1

  • 1Department of Epidemiology and Biostatistics, Indiana University Bloomington, Bloomington, IN 47405, USA.

Bioinformatics (Oxford, England)
|July 5, 2022
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Summary

We developed a multi-trait methylation random field (multi-MRF) method to jointly analyze CpG sites and genetic variants, improving power for disease association studies. This method enhances understanding of methylation patterns and genetic regulation in complex diseases like congenital heart defects.

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Area of Science:

  • Genomics
  • Epigenetics
  • Biostatistics

Background:

  • CpG sites in proximity often exhibit correlated methylation patterns.
  • These patterns are frequently co-regulated by multiple interacting genetic variants.

Purpose of the Study:

  • To introduce a novel multi-trait methylation random field (multi-MRF) method.
  • To evaluate the joint association between sets of CpG sites and genetic variants.
  • To improve statistical power in identifying methylation-based disease associations.

Main Methods:

  • The multi-MRF method employs a multi-trait approach for flexible correlation structures between CpG sites.
  • It integrates effects from multiple common and rare genetic variants (multi-locus).
  • Methylation traits are modeled using a beta distribution to capture bimodal and interval properties.

Main Results:

  • Simulations showed improved power compared to existing methods across various disease scenarios.
  • Application to congenital heart defects (CHDs) identified BACE2 as a methylation quantitative trait locus (QTL) candidate.
  • BACE2 colocalized with expression QTLs and showed nominal associations with CHD in GWAS.

Conclusions:

  • The multi-MRF method offers a powerful approach for joint analysis of methylation data and genetic variants.
  • It provides insights into the genetic regulation of methylation patterns.
  • The findings highlight potential genetic contributors to congenital heart defects through methylation changes.