Standardizing chromatin research: a simple and universal method for ChIP-seq

Arrigoni, Laura; Richter, Andreas S.; Betancourt, Emily; Bruder, Kerstin; Diehl, Sarah; Bönisch, Ulrike

doi:10.1093/nar/gkv1495

Cited by 110 publications

(103 citation statements)

References 37 publications

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“…ChIP-seq experiments still requires protocol improvements for allowing comparable signals (54). Here, we explore computational approaches for ChIP-seq normalization and alternatives to the TMM approach.…”

Section: Resultsmentioning

confidence: 99%

Differential peak calling of ChIP-seq signals with replicates with THOR

et al. 2016

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The study of changes in protein–DNA interactions measured by ChIP-seq on dynamic systems, such as cell differentiation, response to treatments or the comparison of healthy and diseased individuals, is still an open challenge. There are few computational methods comparing changes in ChIP-seq signals with replicates. Moreover, none of these previous approaches addresses ChIP-seq specific experimental artefacts arising from studies with biological replicates. We propose THOR, a Hidden Markov Model based approach, to detect differential peaks between pairs of biological conditions with replicates. THOR provides all pre- and post-processing steps required in ChIP-seq analyses. Moreover, we propose a novel normalization approach based on housekeeping genes to deal with cases where replicates have distinct signal-to-noise ratios. To evaluate differential peak calling methods, we delineate a methodology using both biological and simulated data. This includes an evaluation procedure that associates differential peaks with changes in gene expression as well as histone modifications close to these peaks. We evaluate THOR and seven competing methods on data sets with distinct characteristics from in vitro studies with technical replicates to clinical studies of cancer patients. Our evaluation analysis comprises of 13 comparisons between pairs of biological conditions. We show that THOR performs best in all scenarios.

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Section: Resultsmentioning

confidence: 99%

Differential peak calling of ChIP-seq signals with replicates with THOR

et al. 2016

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“…For NOMe-seq, nuclei of fixed cells were extracted and DNA-meth on GpC motifs in accessible chromatin regions was introduced using the M. CviPI methyltransferase, followed by WGBS analysis. ChIP-seq for histone modifications was carried out as previously described (Arrigoni et al, 2016;Kinkley et al, 2016). RNA was extracted using the miRNeasy Micro Kit (QIAGEN) and three Illumina sequencing libraries were prepared (small RNA sequencing library, one stranded total RNA, and one stranded mRNA library).…”

Section: Experimental Procedures T Cell Isolationmentioning

confidence: 99%

Epigenomic Profiling of Human CD4+ T Cells Supports a Linear Differentiation Model and Highlights Molecular Regulators of Memory Development

Durek¹,

Nordström²,

Gasparoni³

et al. 2016

Immunity

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181

192

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“…Chromatin studies (eg ATAC‐seq, CHIP‐seq) and in vivo genome‐wide mapping of coordinated promoter‐enhancer regulatory activities are possible with intact nuclei. New nuclei isolation methods could reduce input requirements …”

Section: Resultsmentioning

confidence: 99%

The national blueprint for pregnancy/birth longitudinal cohorts to study factor VIII immunogenicity: NHLBI State of the Science (SOS) Workshop on factor VIII inhibitors

Johnsen

Brown

2019

Haemophilia

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Introduction Patients with haemophilia can develop inhibitors to exogenous coagulation factors. Some patients are tolerant to factor, while those who develop inhibitors do so early in life. Genetics and environmental factors are known to contribute to inhibitor risk. However, it is not yet possible to predict inhibitor formation or treatment responsiveness in individuals. We hypothesize that factors in the antenatal/neonatal period inform inhibitor risk development. Aim To consider the design of longitudinal studies beginning in the antenatal/neonatal period and the use of new technologies to better understand haemophilia inhibitors. Methods A working group was formed for the NHLBI State of the Science Workshop: Factor VIII Inhibitors: Generating a National Blueprint for Future Research to solicit input from the US haemophilia community and international collaborators to consider design of pregnancy/birth longitudinal cohorts that leverage ‐omics, existing phenotypic data, and in silico modelling to study inhibitors. Results An antenatal/neonatal longitudinal cohort should begin with enrolment of pregnant genetic carriers of haemophilia and span the at‐risk period for inhibitor development in the child. Data and samples from the mother, placenta, neonate and young child can be obtained that are amenable to existing assays, genomics and other ‐omics studies. Data can inform in silico prediction and mathematical models. Conclusion A longitudinal study beginning before birth offers the unique opportunity to study factors that influence inhibitor development prior to exposure. Advances in ‐omics and computational biology can study complex phenotypes in this rare disease. This study could be accomplished through interdisciplinary efforts and patient community engagement.

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Standardizing chromatin research: a simple and universal method for ChIP-seq

Cited by 110 publications

References 37 publications

Differential peak calling of ChIP-seq signals with replicates with THOR

Differential peak calling of ChIP-seq signals with replicates with THOR

Epigenomic Profiling of Human CD4+ T Cells Supports a Linear Differentiation Model and Highlights Molecular Regulators of Memory Development

The national blueprint for pregnancy/birth longitudinal cohorts to study factor VIII immunogenicity: NHLBI State of the Science (SOS) Workshop on factor VIII inhibitors

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