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The contribution of chromatin accessibility to the risk of inflammatory bowel disease in different p

Nikhil Damle (1), Rohit Aita, BS (1), Manisha Bajpai, PhD (2), Kamilla Deak, BS (2), Sanjana Eranki, BS (2), Oscar Pellon-Cadenas, PhD (1), Claire L. Simpson, PhD (3), Michael Verzi, PhD (1), Steven R. Brant, MD (1,2), Jinchuan Xing, PhD (1) (1)Department of Genetics and the Human Genetics Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, NJ (2)Rutgers Crohns and Colitis Center of New Jersey, Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ 08901 (3)Department of Genetics, Genomics, and Informatics, University of Tennessee Health Science Center, Memphis, TN 38163 USA

Poster # 40

Inflammatory Bowel Disease (IBD) impacts numerous individuals yearly. It is an autoimmune disease that attacks the lining of the digestive tract, leading to digestive issues such as bloating, cramping, and diarrhea. Studies have shown that the prevalence of the disease varies greatly among populations. The underlying molecular mechanisms for the difference in genetic risk of IBD in different populations are still not well-known. Because of this, we hypothesize that chromatin structure may play a role in affecting risk gene accessibility, contributing to the genetic risk variance. Assay of Transposase-Accessible Chromatin (ATAC-seq) is a technology that identifies chromatin accessibility in samples. ATAC-seq profiles can be used to identify differences in chromatin accessibility between different population groups. This will be accomplished through the evaluation of allele-specific transposase-accessible chromatin (asTAC). We hypothesize that at regions associated with differential population disease risk, there will be differential chromatin accessibility profiles that correspond to genetic background. Using 119 ATAC-Seq samples from 32 individuals, we examined the chromatin accessibility in 4 populations. Results from this analysis allow us to understand the population differences at the IBD risk loci.

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