DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ATAC-seq in IMR-32 cells with or without SMARCA4 inactivation. To identify changes in DNA accessibility following SMARCA4 inactivation, we used either the small-molecule catalytic inhibitor BRM014, auxin-induced degradation of IMR-32 cells engineered with SMARCA4 tagged to the minimal auxin-induced degron (SMARCA4-mAID), or the corresponding vehicle controls. Analysis of these locations reveal that SMARCA4-dependent sites are located at enhancers used by the neuroblastoma core regulatory circuitry. Overall design: ATAC-seq in neuroblastoma cells为揭示神经母细胞瘤细胞中SWI/SNF复合物（SWI/SNF Complexes）的全基因组靶标，我们在携带或未携带SMARCA4基因失活的IMR-32细胞中开展了转座酶可及性测序（ATAC-seq）。 为鉴定SMARCA4基因失活后DNA可及性的变化，我们分别采用了三种处理方案：小分子催化抑制剂BRM014处理、对经工程化改造使SMARCA4融合最小生长素诱导降解标签（SMARCA4-mAID）的IMR-32细胞进行生长素诱导降解，以及对应的溶剂空白对照。 对上述位点的分析显示，依赖SMARCA4的染色质位点分布于神经母细胞瘤核心调控环路所使用的增强子区域。 整体实验设计：神经母细胞瘤细胞的ATAC-seq