Journal
EPIGENETICS
Volume 10, Issue 9, Pages 861-871Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15592294.2015.1075691
Keywords
histone H; epigenetics; epigenetic inheritance, high fat diet; obesity; DNA methylation
Funding
- National Cancer Institute, National Institutes of Health [HHSN26120080001E]
- Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research
- National Library of Medicine, NIH
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Several studies have described phenotypic changes in the offspring of mice exposed to a variety of environmental factors, including diet, toxins, and stress; however, the molecular pathways involved in these changes remain unclear. Using a high fat diet (HFD)-induced obesity mouse model, we examined liver gene expression in male offspring and analyzed chromatin of paternal spermatozoa. We found that the hepatic mRNA level of 7 genes (out of 20 evaluated) was significantly altered in HFD male offspring compared to control mice, suggesting that phenotypic changes in the offspring depend on parental diet. We examined 7 imprinted loci in spermatozoa DNA from HFD-treated and control fathers by bisulfite sequencing, but did not detect changes in DNA methylation associated with HFD. Using chromatin immunoprecipitation followed by high-throughput sequencing, we found differential histone H3-occupancy at genes involved in the regulation of embryogenesis and differential H3K4me1-enrichment at transcription regulatory genes in HFD fathers vs. control mice. These results suggest that dietary exposure can modulate histone composition at regulatory genes implicated in developmental processes.
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