ChIPseek, a web-based analysis tool for ChIP data

Chen, Ting-Wen; Li, Hsin Pai; Lee, Chi-Ching; Gan, Ruei Chi; Huang, Po-Jung; Wu, Timothy; Lee, Cheng Yang; Chang, Ian Yi‐Feng; Tang, Petrus

doi:10.1186/1471-2164-15-539

Cited by 60 publications

(51 citation statements)

References 44 publications

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“…The annotation of peaks to the nearest gene was performed using the annotatePeaks.pl function from HOMER [44]. Overrepresented transcription factor binding sites analysis was performed using PscanChip [45], while annotation plots were generated using ChIPseek [46]. Circos plot was generated with Circos [47].…”

Section: Methodsmentioning

confidence: 99%

Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

Pazienza

Panebianco

Rappa

et al. 2016

Epigenetics & Chromatin

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BackgroundObesity has tremendous impact on the health systems. Its epigenetic bases are unclear. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Their role in adipose tissue plasticity is unknown.ResultsHere, we show evidence that macroH2A1.1 protein levels in the visceral adipose tissue of obese humans positively correlate with BMI, while macroH2A1.2 is nearly absent. We thus introduced a constitutive GFP-tagged transgene for macroH2A1.2 in mice, and we characterized their metabolic health upon being fed a standard chow diet or a high fat diet. Despite unchanged food intake, these mice exhibit lower adipose mass and improved glucose metabolism both under a chow and an obesogenic diet. In the latter regimen, transgenic mice display smaller pancreatic islets and significantly less inflammation. MacroH2A1.2 overexpression in the mouse adipose tissue induced dramatic changes in the transcript levels of key adipogenic genes; genomic analyses comparing pre-adipocytes to mature adipocytes uncovered only minor changes in macroH2A1.2 genomic distribution upon adipogenic differentiation and suggested differential cooperation with transcription factors. MacroH2A1.2 overexpression markedly inhibited adipogenesis, while overexpression of macroH2A1.1 had opposite effects.ConclusionsMacroH2A1.2 is an unprecedented chromatin component powerfully promoting metabolic health by modulating anti-adipogenic transcriptional networks in the differentiating adipose tissue. Strategies aiming at enhancing macroH2A1.2 expression might counteract excessive adiposity in humans.Electronic supplementary materialThe online version of this article (doi:10.1186/s13072-016-0098-9) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

Pazienza

Panebianco

Rappa

et al. 2016

Epigenetics & Chromatin

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“…S11) were annotated (using an annotation window of 2 kb upstream of transcriptional start sites [TSSs] and 1 kb downstream of transcriptional termination sites) and analyzed using the ChIPseek tool (Chen et al, 2014). H3K9/ 14ac was almost absent from centromeric and pericentromeric regions (Fig.…”

Section: General Features Of H3k9/14 Acetylationmentioning

confidence: 99%

“…Peaks were annotated by genomic region and nearest gene using the ChIPseek tool (Chen et al, 2014). Heat maps were plotted with the gplots R package (Warnes et al, 2013), and other plots and data selections were created with basic R functions (R Core Team, 2014).…”

Section: Chip-seqmentioning

confidence: 99%

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Nitric Oxide Modulates Histone Acetylation at Stress Genes by Inhibition of Histone Deacetylases

et al. 2016

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Histone acetylation, which is an important mechanism to regulate gene expression, is controlled by the opposing action of histone acetyltransferases and histone deacetylases (HDACs). In animals, several HDACs are subjected to regulation by nitric oxide (NO); in plants, however, it is unknown whether NO affects histone acetylation. We found that treatment with the physiological NO donor S-nitrosoglutathione (GSNO) increased the abundance of several histone acetylation marks in Arabidopsis (Arabidopsis thaliana), which was strongly diminished in the presence of the NO scavenger 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. This increase was likely triggered by NO-dependent inhibition of HDAC activity, since GSNO and S-nitroso-N-acetyl-DL-penicillamine significantly and reversibly reduced total HDAC activity in vitro (in nuclear extracts) and in vivo (in protoplasts). Next, genome-wide H3K9/14ac profiles in Arabidopsis seedlings were generated by chromatin immunoprecipitation sequencing, and changes induced by GSNO, GSNO/2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide or trichostatin A (an HDAC inhibitor) were quantified, thereby identifying genes that display putative NO-regulated histone acetylation. Functional classification of these genes revealed that many of them are involved in the plant defense response and the abiotic stress response. Furthermore, salicylic acid, which is the major plant defense hormone against biotrophic pathogens, inhibited HDAC activity and increased histone acetylation by inducing endogenous NO production. These data suggest that NO affects histone acetylation by targeting and inhibiting HDAC complexes, resulting in the hyperacetylation of specific genes. This mechanism might operate in the plant stress response by facilitating the stress-induced transcription of genes.

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“…In this respect, they represent ideal learning platforms for researchers who would like to make first-hand experiences with ChIP-seq data and familiarize themselves with the corresponding data analysis methods. There are of course other public web servers for ChIP-seq data analysis, for instance Galaxy [5], Cistrome [6], Nebula [7] and ChIPseek [8]. Many of the public data sets accessible through our servers are also viewable at the UCSC genome browser [9].…”

Section: Introductionmentioning

confidence: 99%

Principles of ChIP-seq Data Analysis Illustrated with Examples

Ambrosini

Dreos

Bücher

2015

Genomics Comput Biol

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Chromatin immunoprecipitation (ChIP) followed by high-throughput sequencing (ChIP-seq) is a powerful method to determine how transcription factors and other chromatin-associated proteins interact with DNA in order to regulate gene transcription. A single ChIPseq experiment produces large amounts of highly reproducible data. The challenge is to extract knowledge from the data by thoughtful application of appropriate bioinformatics tools. Here we present a concise introduction into ChIP-seq data analysis in the form of a tutorial based on tools developed by our group. We expose biological questions, explain methods and provide guidelines for the interpretation of the results. While this article focuses on ChIP-seq, most of the algorithms and tools we present are applicable to other chromatin profiling assays based on next generation sequencing (NGS) technology as well.

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ChIPseek, a web-based analysis tool for ChIP data

Cited by 60 publications

References 44 publications

Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

Nitric Oxide Modulates Histone Acetylation at Stress Genes by Inhibition of Histone Deacetylases

Principles of ChIP-seq Data Analysis Illustrated with Examples

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