1. Omics Types

ATAC-Seq

Definition

ATAC-Seq (Assay for Transposase-Accessible Chromatin using sequencing) is an epigenomic technique that maps genome-wide chromatin accessibility by using hyperactive Tn5 transposase to insert sequencing adapters into open chromatin regions. This method identifies regulatory elements such as promoters, enhancers, and transcription factor binding sites by revealing which DNA regions are accessible to regulatory proteins. ATAC-Seq requires fewer cells than alternative methods like DNase-Seq, making it valuable for studying rare cell populations. The resulting accessibility profiles indicate active regulatory regions and can be integrated with gene expression data to understand transcriptional regulation, cell-type-specific programs, and disease mechanisms. ATAC-Seq has become essential for studying chromatin dynamics during development, differentiation, and disease progression.

Visualize ATAC-Seq in Nodes Bio

Researchers can visualize ATAC-Seq data in Nodes Bio by creating networks linking accessible chromatin regions to their target genes and associated transcription factors. Network graphs can integrate chromatin accessibility peaks with gene expression profiles, revealing regulatory hierarchies and identifying master regulators. Users can map how changes in chromatin accessibility correlate with downstream gene expression changes across different conditions or cell types, enabling causal inference of regulatory mechanisms.

Visualization Ideas:

  • Gene regulatory networks connecting accessible chromatin peaks to target genes and transcription factors
  • Multi-omics integration networks combining ATAC-Seq accessibility data with RNA-Seq expression profiles
  • Cell-type-specific regulatory networks showing differential chromatin accessibility across conditions or developmental stages
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Example Use Case

A cancer research team uses ATAC-Seq to compare chromatin accessibility between drug-resistant and drug-sensitive tumor cells. They identify differentially accessible regions near genes involved in drug metabolism and efflux. By integrating ATAC-Seq peaks with RNA-Seq data in a network visualization, they discover that increased accessibility at an enhancer region correlates with upregulation of ABC transporter genes. The network reveals that specific transcription factors binding these accessible regions drive resistance, suggesting new therapeutic targets to overcome drug resistance.

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