DNA methylation within intron 2 of the Stat1 gene is reduced in colon tissue from interleukin-10 gene-deficient mice compared with healthy control mice

Food Nutrition & Health Team, Food & Bio-based Products Group, AgResearch Limited, Palmerston North, New Zealand
Nutrigenomics New Zealand, www.nutrigenomics.org.nz, New Zealand
AgResearch Limited, Palmerston North, New Zealand
Riddet Institute, Massey University, Palmerston North, New Zealand
Gravida: National Centre for Growth and Development, Auckland, New Zealand
DOI
10.7287/peerj.preprints.1391v1
Subject Areas
Molecular Biology, Gastroenterology and Hepatology, Immunology
Keywords
matrix-assisted laser desorption-ionization mass spectrometry, 5 methylcytosine, gene expression, DNA methylation, inflammatory bowel disease
Copyright
© 2015 Barnett et al.
Licence
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ PrePrints) and either DOI or URL of the article must be cited.
Cite this article
Barnett MP, Russ AE, McNabb WC, Roy NC. 2015. DNA methylation within intron 2 of the Stat1 gene is reduced in colon tissue from interleukin-10 gene-deficient mice compared with healthy control mice. PeerJ PrePrints 3:e1391v1

Abstract

Background. Epigenetic influences have been implicated in the development of autoimmunity. While such mechanisms have been linked to mouse models of intestinal inflammation, and to human inflammatory bowel disease (IBD), the involvement of epigenetic mechanisms in the pathogenesis of intestinal inflammation in the interleukin-10 gene-deficient (Il10 –/– ) mouse model of IBD has not yet been reported. This study investigated the hypothesis that changes observed in the expression of Stat1 and Ppara in colon tissue of Il10 –/– mice are associated with differential methylation of CpG sites within key regulatory regions of these genes. Methods. Colon tissue was collected from Il10 –/– and C57BL/6JArc mice at 6 (pre-inflammation) or 12 (established inflammation) weeks of age. Methylation levels of CpG sites within selected regions of the Stat1 and Ppara genes were assessed using MALDI-TOF mass spectrometry in DNA extracted from mouse colon tissue. Results. Methylation of specific CpG sites within intron 2, but not the proximal promoter, of the Stat1 gene was reduced in colon tissue from Il10 –/– mice at 12 weeks of age compared with colon tissue C57BL/6JArc mice at 12 weeks of age. Discussion. These data provide preliminary evidence that DNA methylation is altered in the Il10 –/– mouse model of IBD, and this may be linked with changes in the expression levels of genes that play a key role in inflammation. Further studies are required to confirm these observations, and to establish a causative link between methylation at specific sites (such as intron 2 of Stat1) and gene expression.

Author Comment

This is a preprint submission to PeerJ.

Supplemental Information

Supplementary File 1: The level of methylation at each CpG island for individual mice

DOI: 10.7287/peerj.preprints.1391v1/supp-1