Placental methylome analysis from a prospective autism study

Mol Autism. 2016 Dec 15:7:51. doi: 10.1186/s13229-016-0114-8. eCollection 2016.

Abstract

Background: Autism spectrum disorders (ASD) are increasingly prevalent neurodevelopmental disorders that are behaviorally diagnosed in early childhood. Most ASD cases likely arise from a complex mixture of genetic and environmental factors, an interface where the epigenetic marks of DNA methylation may be useful as risk biomarkers. The placenta is a potentially useful surrogate tissue characterized by a methylation pattern of partially methylated domains (PMDs) and highly methylated domains (HMDs) reflective of methylation patterns observed in the early embryo.

Methods: In this study, we investigated human term placentas from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) prospective study by whole genome bisulfite sequencing. We also examined the utility of PMD/HMDs in detecting methylation differences consistent with ASD diagnosis at age three.

Results: We found that while human placental methylomes have highly reproducible PMD and HMD locations, there is a greater variation between individuals in methylation levels over PMDs than HMDs due to both sampling and individual variability. In a comparison of methylation differences in placental samples from 24 ASD and 23 typically developing (TD) children, a HMD containing a putative fetal brain enhancer near DLL1 was found to reach genome-wide significance and was validated for significantly higher methylation in ASD by pyrosequencing.

Conclusions: These results suggest that the placenta could be an informative surrogate tissue for predictive ASD biomarkers in high-risk families.

Keywords: Biomarkers; DNA methylation; Epigenetics; Genomics; Methylome; Placenta.

MeSH terms

  • Autism Spectrum Disorder / diagnosis*
  • Autism Spectrum Disorder / genetics
  • Biomarkers / metabolism
  • Calcium-Binding Proteins
  • Child, Preschool
  • DNA Methylation
  • Early Diagnosis
  • Enhancer Elements, Genetic*
  • Epigenesis, Genetic*
  • Female
  • Genome, Human
  • Genome-Wide Association Study
  • High-Throughput Nucleotide Sequencing
  • Humans
  • Infant, Newborn
  • Intercellular Signaling Peptides and Proteins / genetics*
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Male
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Placenta / metabolism*
  • Pregnancy

Substances

  • Biomarkers
  • Calcium-Binding Proteins
  • DLK1 protein, human
  • Intercellular Signaling Peptides and Proteins
  • Membrane Proteins