{"id":1560,"date":"2022-09-23T20:35:10","date_gmt":"2022-09-23T20:35:10","guid":{"rendered":"https:\/\/labs.icahn.mssm.edu\/roussos-lab\/?page_id=1560"},"modified":"2022-09-25T13:29:40","modified_gmt":"2022-09-25T13:29:40","slug":"atacad","status":"publish","type":"page","link":"https:\/\/labs.icahn.mssm.edu\/roussos-lab\/atacad\/","title":{"rendered":"The three-dimensional landscape of chromatin accessibility in Alzheimer’s disease"},"content":{"rendered":"

To characterize the dysregulation of chromatin accessibility in Alzheimer\u2019s disease (AD), we generated 636 ATAC-seq libraries in neurons and non-neurons isolated from the superior temporal gyrus and entorhinal cortex of 153 AD cases and 56 controls. By analyzing a total of ~20 billion read pairs, we expanded the repertoire of known open chromatin regions (OCRs) in the human brain and identified cell type-specific enhancer-promoter interactions. We show that inter-individual variability in OCRs can be leveraged to identify cis-regulatory domains (CRDs) that capture the three-dimensional structure of the genome (3D genome). We identified AD-associated effects on chromatin accessibility, the 3D genome and transcription factor regulatory networks. For one of the most AD-perturbed transcription factors, USF2, we validated its regulatory effect on lysosomal genes. Overall, we applied a systematic approach to understand the role of the 3D genome in AD. We provide all data as an online resource for widespread community-based analysis.<\/p>\n

Data: Raw data & UCSC hub<\/h2>\n

Raw and processed data are available at Synapse<\/a>. You can also view the open chromatin tracks in the UCSC genome browser<\/strong> as a track hub:<\/p>\n