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This article is part of the supplement: UT-ORNL-KBRIN Bioinformatics Summit 2009

Open Access Meeting abstract

Extensive parent-of-origin genetic effects on fetal growth

Ronald M Adkins1*, Julia Krushkal2, Grant Somes2, John Fain3, John Morrison4, Chad Klauser4 and Everett F Magann5

Author affiliations

1 Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, USA

2 Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA

3 Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA

4 Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS 39216, USA

5 Department of Obstetrics and Gynecology, Naval Medical Center at Portsmouth, VA 23708, USA

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Citation and License

BMC Bioinformatics 2009, 10(Suppl 7):A13  doi:10.1186/1471-2105-10-S7-A13

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2105/10/S7/A13


Published:25 June 2009

© 2009 Adkins et al; licensee BioMed Central Ltd.

Background

Epigenetic effects have recently been recognized as playing a very significant role in several normal and pathological phenotypes. Imprinting, the silencing of either the paternally or maternally inherited allele, is one of the most pervasive and consistent epigenetic mechanisms across species and individuals. The majority of imprinted loci are involved in fetal growth regulation, and several defects in the epigenetic regulation of these genes are associated with extremes of fetal growth.

Materials and methods

We surveyed 62 SNPs across 17 genes (Table 1) in a cohort of African-American mother-newborn pairs selected using stringent inclusion/exclusion criteria intended to enrich for the genetic component of fetal growth regulation. All association analyses were adjusted for admixture using a suite of ancestry informative SNP markers. By inferring haplotypes within the imprinted loci in mothers and newborns, we could unambiguously infer the parental origin of haplotypes and associated alleles in the majority of newborns.

Table 1. SNPs Genotyped

Results and conclusion

We found very significant parent-of-origin effects in the insulin, H19 and GNAS genes that were completely consistent with their known patterns of imprinting. In the case of the insulin polymorphisms, a consistent trend was also observed for newborn IGF-II levels with respect to parental origin of haplotypes.

Acknowledgements

This work was supported by grants to RMA from the National Institute of Child Health and Human Development (HD055462), the Children's Foundation Research Center of Memphis, the University of Tennessee Health Science Center's Clinical Translational Science Institute, and the Accredo Foundation. Support was also provided to GS from The Urban Child Institute to support the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) study.