Environmental Epigenetics

Program Description

The organization of DNA into chromatin presents the cell with the opportunity to use powerful regulatory mechanisms broadly defined as epigenetics. Research designed to characterize the molecular basis of disease tends to be gene-centric and may therefore miss important sources of variation. Increasing evidence demonstrates that epigenetic mechanisms are linked to gene activation, gene silencing and chromosomal instability. Thus, a purely DNA sequence-based approach (naked DNA snapshot) may not be sufficient to explain pathogenesis of diseases that have a heritable component, but are modulated by other non-genetic or extra-genetic mechanisms.

The goal of this program is to advance the concept of gene-environment interaction in diseases to the study of alteration in gene expression as influenced by environmental exposures with the elucidation of epigenetic mechanisms responsible for altered gene expression. This program supports the examination of several aspects of epigenetic regulation, from imprinting, to DNA methylation at promoter or other sites, to chromatin modifications, to gene silencing induced by siRNA, and other novel epigenetic mechanisms, for a role in disease and dysfunction with an environmental exposure component. State-of-the-art technologies are being employed to analyze the epigenetic changes in single genes, signaling pathways or the entire genome in response to exposure. Investigators are using in vivo animal models, in vitro cell cultures, human tissues and/or biologic samples to examine epigenetic changes and to determine the precise mechanism responsible for the change. Awards to grants in this program were made in 2006.

Program Contacts

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