Creating 2D Occupancy Plots Using plot2DO

Beati, Paula; Chereji, Răzvan V.

doi:10.1007/978-1-0716-0301-7_5

Cited by 14 publications

(19 citation statements)

References 16 publications

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Section: Resultssupporting

confidence: 88%

“…Considering the NucleoATAC model inputs, we hypothesized that this was the result of differences in nucleosome-length fragments mapping to P3F sites, where a relative depletion of longer nucleosomal vs. shorter sub-nucleosomal fragments would result in low confidence nucleosome occupancy scores. Using plot2DO (Beati and Chereji, 2020), we in fact observed differences in fragment length distributions consistent with our NucleoATAC result (Figure 2G). We interpret this anomaly in nucleosome-length fragment distribution as evidence of local nucleosome redistribution taking place during the transition between baseline (t0) and P3F-driven epigenetic equilibrium (t24).…”

Section: Cellular and Genomic Localization Of The Pax3-foxo1 Fusion Transcription Factor To Inactive Chromatinsupporting

confidence: 87%

“…After peaks are called, heatmaps are generated with deeptools (version 3.3.1) (Ramirez et al, 2016). Fragment length distributions were generated with plot2DO v1.0 (https://github.com/rchereji/plot2DO) (Beati and Chereji, 2020). Local signal vs background enrichment is calculated with localEnrichmentBed (https://github.com/dariober/bioinformaticscafe/tree/master/localEnrichmentBed).…”

Section: Atac-seq and Atac-seq Data Analysismentioning

confidence: 99%

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Pioneer activity of an oncogenic fusion transcription factor at inaccessible chromatin

Sunkel

Wang

LaHaye

et al. 2020

Preprint

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Recent advances in the characterization of pioneer factors have led to new questions about domain structures and chromatin recognition. Seemingly separate fields have integrated common scientific problems with the identification of fusion pioneer factor (PF) pairs in childhood cancers. Excitingly, this represents a convergence of fields within science, of pediatric oncology, genomics, epigenetics, and biophysics. With PF-pairs emerging as driver oncogenes in childhood rhabdomyosarcoma (RMS), our studies investigate these fusion genes as a gestalt phenomenon, where the whole might equal more than the sum of the parts. We developed a new method for ChIP-seq with per-cell normalization (pc-ChIP-seq) to simultaneously define genome size and PAX3-FOXO1 localization in RMS. We report novel pioneer function for the major driver oncogene in RMS, with nucleosome-motif targeting and kinetic displacement of nucleosomes in human cells.

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Section: Resultssupporting

confidence: 88%

Section: Cellular and Genomic Localization Of The Pax3-foxo1 Fusion Transcription Factor To Inactive Chromatinsupporting

confidence: 87%

Section: Atac-seq and Atac-seq Data Analysismentioning

confidence: 99%

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Pioneer activity of an oncogenic fusion transcription factor at inaccessible chromatin

Sunkel

Wang

LaHaye

et al. 2020

Preprint

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“…In Figures 4 and S4, Plot2DO (Beati and Chereji, 2020) revision number 87fadb4acd23214f83e5440b0ccb02c623fa62d9 with parameters "-t dyads -r Plus1 -l 100 -L 400 -m 0.02" was used to generate 2DO heatmaps from the MNase-ChIP-seq data. In some analyzes, the fragments not overlapping the top 10% of genes were removed using seqtools with command "seqtools intersecta Top10percentTxbdGenes.txt", where "Top10percentTxbdGenes.txt" contains the top 10% most transcribed genes and their coordinates.…”

Section: Two-dimensional Occupancy (2do) Plotsmentioning

confidence: 99%

FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner

Jeronimo

Angel

Poitras

et al. 2020

Preprint

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The histone chaperone FACT occupies transcribed regions where it plays prominent roles in maintaining chromatin integrity and preserving epigenetic information. How it is targeted to transcribed regions, however, remains unclear. Proposed models for how FACT finds its way to transcriptionally active chromatin include docking on the RNA polymerase II (RNAPII) C-terminal domain (CTD), recruitment by elongation factors, recognition of modified histone tails and binding partially disassembled nucleosomes. Here, we systematically tested these and other scenarios in Saccharomyces cerevisiae and found that FACT binds transcribed chromatin, not RNAPII. Through a combination of experimental and mathematical modeling evidence, we propose that FACT recognizes the +1 nucleosome, as it is partially unwrapped by the engaging RNAPII, and spreads to downstream nucleosomes aided by the chromatin remodeler Chd1. Our work clarifies how FACT interacts with genes, suggests a processive mechanism for FACT function, and provides a framework to further dissect the molecular mechanisms of transcription-coupled histone chaperoning.

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“…Figure 1). Only a few tools have been developed that can easily generate V-plots (Beati & Chereji, 2020;Schep et al, 2015), and they are provided as scripts to be used with the command-line interface. Thus, they lack the customization and interaction with other datasets typically available in the wealthy R/Bioconductor environment.…”

Section: Statement Of Needmentioning

confidence: 99%