Date event : March 16, 2018 - 1:00pm Conference / Talk Published on 02/21/2018 - 9:12am
Our laboratory aims to understand how genetics and environment contribute to phenotypic variation. In this regard, we are building on the hypothesis that some of these effects integrate at the epigenetic level thereby contributing to phenotypic display. By monitoring epigenetic changes in specific cell types, we aim to reveal the underlying molecular mechanisms that contribute to phenotype, with a focus on neuro and immune diseases. To this end, we have developed a functional genomics approach (Histone H3 K27 acetylation ChIP-seq) to detect genome-wide epigenetic variation in patients and control cohorts. I will demonstrate feasibility of our approach with studies on different diseases, including Autism spectrum disorder and Tuberculosis. Characterization of gene regulatory alterations in these studies revealed previously known and unknown disease mechanisms. For example, we identified disease genes because they were highly dysregulated at the epigenetic level. In addition, we discovered genetic variants acting via cell type specific gene regulatory regions. Although our approach does not reveal whether the observed molecular mechanisms are caused by prior life events or whether they are causal or correlated, this strategy reveals disease mechanisms in an unbiased and cell type specific manner. I will conclude by describing our vision of how to further study epigenetic mechanisms to better understand how phenotypic variation contributes to disease.
Friday 16 March, 1pm, SBRI conference room.
Invited by Irene Aksoy