Detect accessible chromatin using ATAC-sequencing, from principle to applications

Sun, Yuanyuan; Miao, Nan; Sun, Tao

doi:10.1186/s41065-019-0105-9

Cited by 62 publications

(56 citation statements)

References 128 publications

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“…Since we identified APH DOWN genes in RKO cells involved in chromatin and nucleosome organization, we examined the impact of aphidicolin on chromatin structure by performing the Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq), a method for assaying chromatin accessibility genome-wide (62,63). We observed a global remodelling of chromatin accessibility under aphidicolin treatment demonstrated by a lower strength of ATAC-seq peaks and an increase ATAC-seq peaks coverage in both Early and Late replicated genomic regions ( Figure S5c,f).…”

Section: Aphidicolin Modulates Chromatin Accessibility Within Adv Artilmentioning

confidence: 99%

Low replication stress leads to specific replication timing advances associated to chromatin remodelling in cancer cells

Courtot

Bournique

Maric

et al. 2020

Preprint

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DNA replication is very well orchestrated in mammalian cells due to a tight regulation of the temporal order of replication origin activation, known as the replication timing program. The replication timing of a given replication domain is very robust and well conserved in each cell type. Upon low replication stress, the slowing of replication forks induces delayed replication of some fragile regions leading to DNA damage and genetic instability. Except for these fragile regions, the direct impact of low replication stress on the replication timing in different cellular backgrounds has not been explored in detail. Here we analysed DNA replication timing across the whole genome in a panel of human cell lines in the presence of low replication stress. We demonstrate that low replication stress induced by aphidicolin has a stronger impact on the replication timing of cancer cells than non-tumour cells. Strikingly, we unveiled an enrichment of specific replication domains undergoing a switch from late to early replication in some cancer cells. We found that advances in replication timing correlate with heterochromatin regions poorly sensitive to DNA damage signalling while being subject to an increase of chromatin accessibility in response to aphidicolin. Finally, our data indicate that, following release from replication stress conditions, replication timing advances can be inherited by the next cellular generation, suggesting a new mechanism by which some cancer cells would adapt to cellular or environmental stress.

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Section: Aphidicolin Modulates Chromatin Accessibility Within Adv Artilmentioning

confidence: 99%

Low replication stress leads to specific replication timing advances associated to chromatin remodelling in cancer cells

Courtot

Bournique

Maric

et al. 2020

Preprint

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Section: Discussionmentioning

confidence: 99%

“…ATAC-Seq might also be expected to contain fewer bands than FS-Seq with the bands present being located primarily in the regulatory region (4). Although originally developed as an alternative or complement to MN-Seq, ATAC-Seq is now generally used as a way to identify open chromatin (4). Since SV40 chromatin typically has an open region associated with the regulatory region, it is not surprising that the brightest bands in the heatmap are found in the regulatory region using ATAC-Seq with very few bands in the coding regions.…”

Section: Discussionmentioning

confidence: 99%

“…For example, for micrococcal nuclease the concentration of enzyme and length of digestion must be titrated for each batch of chromatin in order to obtain optimal digestion for studying nucleosomes (3). As described above ATAC-Seq is very sensitive to higher-order structure and for this reason is used primarily to investigate regions of open chromatin (4). ChIP-Seq while a very powerful technique to locate nucleosomes carrying a modified histone of interest does not generate information about nucleosome location lacking the modified histone of interest (5).…”

Section: Introductionmentioning

confidence: 99%

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Mapping the Location of Nucleosomes in Simian Virus 40 Chromatin Using the New England Biolabs FS Library Prep Kit

Milavetz

Haugen

Rowbotham

2020

Preprint

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The location of nucleosomes in chromatin significantly impacts many biological processes including DNA replication, repair and gene expression. A number of techniques have been developed for mapping nucleosome locations in chromatin including MN-Seq (micrococcal nuclease digestion followed by next generation sequencing), ATAC-Seq (Tagamet chromatin fragmentation followed by next generation sequencing), and ChIP-Seq (chromatin immunoprecipitation and fragmentation followed by next generation sequencing). All of these techniques have been successfully used, but each with its own limitations. Recently, New England Biolabs has marketed a new kit, the NEBNext UltraII FS Library Prep kit, for preparing libraries for next generation sequencing from purified genomic DNA. This kit is based on a novel proprietary DNA fragmentation procedure which appears to cleave DNA that is not bound by proteins. Because DNA is fragmented directly in the FS kit, we tested whether the kit might also be useful for mapping the location of nucleosomes in chromatin. Using Simian Virus 40 (SV40) chromatin isolated at different times in an infection, we have compared nucleosome mapping using the NEB FS kit (FS-Seq) to MN-Seq, ATAC-Seq, and ChIP-Seq. Mapping nucleosomes using FS-Seq generated nucleosome profiles similar to those generated by ATAC-Seq and ChIP-Seq in regulatory regions of the SV40 genome. We conclude that FS-Seq is a simple, robust, cost-effective procedure for mapping nucleosomes in SV40 chromatin that should be useful for other forms of chromatin as well. We also present evidence that the FS kit may be useful for mapping the location of transcription factors in chromatin when sequencing reads between 75 and 99 base pairs in size are analyzed.

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“…transcription factor binding sites), which are collectively the targets 35 of defined trans-acting factors (e.g. transcription factors) (4). Aggregating reads in these ways 36 allows for a comparison of accessibility variation between samples and inference of the 37 chromatin landscape of cell populations.…”

mentioning

confidence: 99%

Matrix factorization and transfer learning uncover regulatory biology across multiple single-cell ATAC-seq data sets

Erbe¹,

Kess²,

ler³

et al. 2020

Preprint

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AbstractWhile single-cell ATAC-seq analysis methods allow for robust clustering of cell types, the question of how to integrate multiple scATAC-seq data sets and/or sequencing modalities is still open. We present an analysis framework that enables such integration by applying the CoGAPS Matrix Factorization algorithm and the projectR transfer learning program to identify common regulatory patterns across scATAC-seq data sets. Using publicly available scATAC-seq data, we find patterns that accurately characterize cell types both within and across data sets. Furthermore, we demonstrate that these patterns are both consistent with current biological understanding and reflective of novel regulatory biology.

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Detect accessible chromatin using ATAC-sequencing, from principle to applications

Cited by 62 publications

References 128 publications

Low replication stress leads to specific replication timing advances associated to chromatin remodelling in cancer cells

Low replication stress leads to specific replication timing advances associated to chromatin remodelling in cancer cells

Mapping the Location of Nucleosomes in Simian Virus 40 Chromatin Using the New England Biolabs FS Library Prep Kit

Matrix factorization and transfer learning uncover regulatory biology across multiple single-cell ATAC-seq data sets

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