ATAC-seq Services

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Accessible chromatin analysis at your fingertips

  • Detects 3X more reads on open chromatin *
  • Accurate results with high reproducibility between replicates
  • Comprehensive bioinformatic analysis in a publication-ready report
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What is ATAC-seq?

ATAC-seq stands for Assay for Transposase-Accessible Chromatin with high-throughput sequencing, which is a convenient method to gather genomic information. Specifically, ATAC-seq maps regions of the genome that have open chromatin, that is, regions not occupied by nucleosomes or transcription factors. Open chromatin regions can be linked to epigenetic gene regulation, making ATAC-seq a valuable tool for multiple research fields. ATAC-seq has been used in multiple fields of scientific research ranging from pharmacological studies in immunology[2], neurobiology[3], cardiovascular diseases[4], single-cell chromatin accessibility studies[5,6], and others.

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3-Fold Increase in Reads at Accessible Chromatin Regions

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Percent of reads retained after filtering for low quality, mitochondria and duplicates

Novel chemistry retains 3 times more reads by :

  • Decreasing mitochondrial contamination
  • Decreasing duplicated reads
  • Providing high coverage of accessible nuclear DNA

High Reproducibility Between Peaks Called for Replicates

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MACS2 was used to call peaks for two biological replicates. The peaks were compared using Bedtools intersect with minimum overlap of 0.5 to determine how many common peaks were present in both replicates.

Zymo-seq ATAC Peaks Highly Matched DNase I Peaks

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BigWig files for Zymo-seq ATAC and DNase-seq from ENCODE were uploaded to IGV [7]

Ready-To-Publish Data at the Touch of a Button

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Complete analysis includes :

  • Peak calling and differential analysis
  • Peak annotation for genomic regions
  • Fraction of reads in peaks (FRiP score)
  • Fragment size distribution plot
  • Sequence quality QC
  • Downloadable files: fastq, BAM, BigWig, Peaks genomic coordinates
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* comparing to the standard protocol[1]

[1] Buenrostro, Jason D., et al. “Transposition of native chromatin for fast and sensitive epigenomic profiling of open chromatin, DNAbinding proteins and nucleosome position.” Nature methods 10.12 (2013): 1213.
[2] Pereira, Renata M., et al. “Transcriptional and epigenetic regulation of T cell hyporesponsiveness.” Journal of leukocyte biology 102.3 (2017): 601-615.
[3] Su, Yijing, et al. “Neuronal activity modifies the chromatin accessibility landscape in the adult brain.” Nature neuroscience 20.3 (2017): 476.
[4] Costantino, Sarah, et al. “Epigenetics and precision medicine in cardiovascular patients: from basic concepts to the clinical
arena.” European heart journal 39.47 (2017): 4150-4158.
[5] Cusanovich, Darren A., et al. “Multiplex single-cell profiling of chromatin accessibility by combinatorial cellular indexing.” Science 348.6237 (2015): 910-914.
[6] Buenrostro, Jason D., et al. “Single-cell chromatin accessibility reveals principles of regulatory variation.” Nature 523.7561 (2015): 486.
[7] James T. Robinson, Helga Thorvaldsdóttir, Aaron M. Wenger, Ahmet Zehir, Jill P. Mesirov. Variant Review with the Integrative Genomics Viewer (IGV). Cancer Research 77(21) 31-34 (2017).