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Genotype-Epigenotype Interaction at the IGF2 DMR.

Susan K Murphy1, Erin Erginer2, Zhiqing Huang3

  • 1Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Duke University Medical Center, Box 91012, B223 LSRC Building, Durham, NC 27708, USA. susan.murphy@duke.edu.

Genes
|September 8, 2015
PubMed
Summary

A genetic variation in the Insulin-like Growth Factor II (IGF2) gene

Keywords:
CpG dinucleotideInsulin-like Growth Factor IIdifferentially methylated regionhypomethylationimprinted genepolymorphism

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Area of Science:

  • Genetics
  • Epigenetics
  • Molecular Biology

Background:

  • Insulin-like Growth Factor II (IGF2) is a growth-promoting gene paternally expressed.
  • IGF2 overexpression is linked to various disorders and diseases.
  • IGF2 regulation involves differential methylation of its alleles, particularly at the upstream differentially methylated region (DMR).

Purpose of the Study:

  • To investigate the impact of genetic variations on IGF2 methylation.
  • To identify novel sources of IGF2 hypomethylation beyond environmental factors.
  • To understand the interplay between genetic and epigenetic regulation of IGF2.

Main Methods:

  • Bisulfite pyrosequencing to analyze DNA methylation.
  • Nucleotide sequencing to confirm genetic variations.
  • Analysis of a specific CpG to CpC transversion within the IGF2 DMR.

Main Results:

  • A CpG to CpC transversion was identified in the IGF2 DMR.
  • This transversion leads to hypomethylation of a CpG site within the DMR.
  • The genetic variation acts as an additive source of hypomethylation, independent of environmental influences.

Conclusions:

  • A genetic polymorphism can cause IGF2 hypomethylation, contributing to disease risk.
  • This finding highlights a genetic basis for epigenetic alterations in IGF2 regulation.
  • The study reveals an additive effect of genetic and non-genetic factors on IGF2 methylation patterns.