Zerone: a ChIP-seq discretizer for multiple replicates with built-in quality control

Cuscó, Pol; Filion, Guillaume J.

doi:10.1093/bioinformatics/btw336

Cited by 11 publications

(7 citation statements)

References 24 publications

(25 reference statements)

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“…ChIP-seq reads were mapped on GRCh37/hg19 with BWA-MEM with default parameters and a minimum mapping quality of 20. The targets were identified with Zerone v1.0 ( 54 ) with options ‘–list-output’ and ‘–confidence 0.99’.…”

Section: Methodsmentioning

confidence: 99%

The chromatin landscape at the HIV-1 provirus integration site determines viral expression

Vansant

Chen

Zorita

et al. 2020

Nucleic Acids Research

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HIV-1 persists lifelong in memory cells of the immune system as latent provirus that rebounds upon treatment interruption. Therefore, the latent reservoir is the main target for an HIV cure. Here, we studied the direct link between integration site and transcription using LEDGINs and Barcoded HIV-ensembles (B-HIVE). LEDGINs are antivirals that inhibit the interaction between HIV-1 integrase and the chromatin-tethering factor LEDGF/p75. They were used as a tool to retarget integration, while the effect on HIV expression was measured with B-HIVE. B-HIVE tracks insert-specific HIV expression by tagging a unique barcode in the HIV genome. We confirmed that LEDGINs retarget integration out of gene-dense and actively transcribed regions. The distance to H3K36me3, the marker recognized by LEDGF/p75, clearly increased. LEDGIN treatment reduced viral RNA expression and increased the proportion of silent provirus. Finally, silent proviruses obtained after LEDGIN treatment were located further away from epigenetic marks associated with active transcription. Interestingly, proximity to enhancers stimulated transcription irrespective of LEDGIN treatment, while the distance to H3K36me3 only changed after treatment with LEDGINs. The fact that proximity to these markers are associated with RNA expression support the direct link between provirus integration site and viral expression.

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Section: Methodsmentioning

confidence: 99%

The chromatin landscape at the HIV-1 provirus integration site determines viral expression

Vansant

Chen

Zorita

et al. 2020

Nucleic Acids Research

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“…The bdgcmp function of MACS2 was used to refine the resulting peaks using the ‘Poisson Pvalue’ (ppois) method. Aligned reads were discretized using Zerone (version 1.0) ( 50 ). The discretized profiles were then used to generate scatter plots.…”

Section: Methodsmentioning

confidence: 99%

A c-Myb mutant causes deregulated differentiation due to impaired histone binding and abrogated pioneer factor function

Fuglerud

Lemma

Wanichawan

et al. 2017

Nucleic Acids Research

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The transcription factor c-Myb is involved in early differentiation and proliferation of haematopoietic cells, where it operates as a regulator of self-renewal and multi-lineage differentiation. Deregulated c-Myb plays critical roles in leukaemias and other human cancers. Due to its role as a master regulator, we hypothesized it might function as a pioneer transcription factor. Our approach to test this was to analyse a mutant of c-Myb, D152V, previously reported to cause haematopoietic defects in mice by an unknown mechanism. Our transcriptome data from K562 cells indicates that this mutation specifically affects c-Myb's ability to regulate genes involved in differentiation, causing failure in c-Myb's ability to block differentiation. Furthermore, we see a major effect of this mutation in assays where chromatin opening is involved. We show that each repeat in the minimal DNA-binding domain of c-Myb binds to histones and that D152V disrupts histone binding of the third repeat. ATAC-seq data indicates this mutation impairs the ability of c-Myb to cause chromatin opening at specific sites. Taken together, our findings support that c-Myb acts as a pioneer factor and show that D152V impairs this function. The D152V mutant is the first mutant of a transcription factor specifically destroying pioneer factor function.

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“…Mapping and disambiguation were performed as explained in the section Allele-Specific Analysis. Peak calling was performed using Zerone (Cuscó and Filion, 2016), i h op ion make a ac a compile time. The ATAC-seq profiles were discretized using default parameters against the baseline set by the NPC profile.…”

Section: Atac-seq Analysismentioning

confidence: 99%

Chromosome Compartments on the Inactive X Guide TAD Formation Independently of Transcription during X-Reactivation

Bauer

Vidal

Zorita

et al. 2020

Preprint

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SummaryA hallmark of chromosome organization is the partition into transcriptionally active A and repressed B compartments and into topologically associating domains (TADs). Both structures were regarded absent from the inactive X chromosome, but to be re-established with transcriptional reactivation and chromatin opening during X-reactivation. Here, we combine a tailor-made mouse iPSC-reprogramming system and high-resolution Hi-C to produce the first time-course combining gene reactivation, chromatin opening and chromosome topology during X-reactivation. Contrary to previous observations, we uncover A/B-like compartments on the inactive X harboring multiple subcompartments. While partial X-reactivation initiates within a compartment rich in X-inactivation escapees, it then occurs rapidly along the chromosome, coinciding with acquisition of naive pluripotency, leading to downregulation of Xist. Importantly, we find that TAD formation precedes transcription, suggesting them to be causally independent. Instead, TADs form first within Xist-poor compartments, establishing Xist as common denominator, opposing both gene reactivation and TAD formation through separate mechanisms.Graphical Summary

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Zerone: a ChIP-seq discretizer for multiple replicates with built-in quality control

Cited by 11 publications

References 24 publications

The chromatin landscape at the HIV-1 provirus integration site determines viral expression

The chromatin landscape at the HIV-1 provirus integration site determines viral expression

A c-Myb mutant causes deregulated differentiation due to impaired histone binding and abrogated pioneer factor function

Chromosome Compartments on the Inactive X Guide TAD Formation Independently of Transcription during X-Reactivation

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