scholarly journals Comparative Analysis of Histone H3K4me3 Distribution in Mouse Liver in Different Diets Reveals the Epigenetic Efficacy of Cyanidin-3-O-glucoside Dietary Intake

2021 ◽  
Vol 22 (12) ◽  
pp. 6503
Author(s):  
Giuseppe Persico ◽  
Francesca Casciaro ◽  
Alessandra Marinelli ◽  
Chiara Tonelli ◽  
Katia Petroni ◽  
...  
Keyword(s):  
Chromatin Immunoprecipitation ◽  
Wide Distribution ◽  
Metabolic Reprogramming ◽  
High Fat ◽  
Yellow Corn ◽  
Genome Wide ◽  
Epigenetic Signal ◽  
Chromatin Immunoprecipitation Sequencing ◽  
Genomic Reprogramming ◽  
One Year

Background: Different diets result in significantly different phenotypes through metabolic and genomic reprogramming. Epigenetic marks, identified in humans and mouse models through caloric restriction, a high-fat diet or the intake of specific bioactives, suggest that genomic reprogramming drives this metabolic reprogramming and mediates the effect of nutrition on health. Histone modifications encode the epigenetic signal, which adapts genome functions to environmental conditions, including diets, by tuning the structure and properties of chromatin. To date, the effect of different diets on the genome-wide distribution of critical histone marks has not been determined. Methods: Using chromatin immunoprecipitation sequencing, we investigated the distribution of the trimethylation of lysine 4 of histone H3 in the liver of mice fed for one year with five different diets, including: chow containing yellow corn powder as an extra source of plant bioactives or specifically enriched with cyanidin-3-O-Glucoside, high-fat-enriched obesogenic diets, and caloric-restricted pro-longevity diets. Conclusions: Comparison of the resulting histone mark profiles revealed that functional food containing cyanidin determines a broad effect.

scholarly journals Genome-wide dysregulation of histone acetylation in the Parkinson’s disease brain

2019 ◽  
Author(s):  
Lilah Toker ◽  
Gia T Tran ◽  
Janani Sundaresan ◽  
Ole-Bjørn Tysnes ◽  
Guido Alves ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Chromatin Immunoprecipitation ◽  
Genetic Risk ◽  
Neurodegenerative Disorder ◽  
Unknown Etiology ◽  
Transcriptomic Data ◽  
Genome Wide ◽  
A Genome ◽  
Chromatin Immunoprecipitation Sequencing ◽  
Epigenetic Signatures

AbstractParkinson disease (PD) is a complex neurodegenerative disorder of largely unknown etiology. While several genetic risk factors have been identified, the involvement of epigenetics in the pathophysiology of PD is mostly unaccounted for. We conducted a histone acetylome-wide association study in PD, using brain tissue from two independent cohorts of cases and controls. Immunoblotting revealed increased acetylation at several histone sites in PD, with the most prominent change observed for H3K27, a marker of active promoters and enhancers. Chromatin immunoprecipitation sequencing (ChIP-seq) further indicated that H3K27 hyperacetylation in the PD brain is a genome-wide phenomenon, with a strong predilection for genes implicated in the disease, including SNCA, PARK7, PRKN and MAPT. Integration of the ChIP-seq with transcriptomic data revealed that the correlation between promoter H3K27 acetylation and gene expression is attenuated in PD patients, suggesting that H3K27 acetylation may be decoupled from transcription in the PD brain. Our findings strongly suggest that dysregulation of histone acetylation plays an important role in the pathophysiology of PD and identify novel epigenetic signatures associated with the disease.

scholarly journals Fast Detection of Differential Chromatin Domains with SCIDDO

2018 ◽  
Author(s):  
Peter Ebert ◽  
Marcel H. Schulz
Keyword(s):  
Histone Modifications ◽  
Chromatin Immunoprecipitation ◽  
Regulatory Elements ◽  
Differential Analysis ◽  
Chromatin Domains ◽  
Chromatin Dynamics ◽  
Fast Detection ◽  
Genome Wide ◽  
Chromatin Immunoprecipitation Sequencing

AbstractThe generation of genome-wide maps of histone modifications using chromatin immunoprecipitation sequencing (ChIP-seq) is a common approach to dissect the complexity of the epigenome. However, interpretation and differential analysis of histone ChIP-seq datasets remains challenging due to the genomic co-occurrence of several marks and their difference in genomic spread. Here we present SCIDDO, a fast statistical method for the detection of differential chromatin domains (DCDs) from chromatin state maps. DCD detection simplifies relevant tasks such as the characterization of chromatin changes in differentially expressed genes or the examination of chromatin dynamics at regulatory elements. SCIDDO is available at github.com/ptrebert/sciddo

scholarly journals Angioplasty-induced epigenomic remodeling entails BRD4 and EZH2 hierarchical regulations

2020 ◽  
Author(s):  
Mengxue Zhang ◽  
Bowen Wang ◽  
Go Urabe ◽  
Hatice Gulcin Ozer ◽  
Renzhi Han ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Chromatin Immunoprecipitation ◽  
Carotid Arteries ◽  
Neointimal Hyperplasia ◽  
Epigenetic Factors ◽  
Genome Wide ◽  
Ezh2 Expression ◽  
Chromatin Immunoprecipitation Sequencing ◽  
Genome Wide Survey

AbstractAtherosclerosis is commonly treated with angioplasty which, however, evokes neointimal hyperplasia (IH) and recurrent stenotic diseases. Epigenomic investigation was lacking on post-angioplasty IH. The histone acetylation reader BRD4 and H3K27me3 writer EZH2 are potent epigenetic factors; their relationship is little understood. Through genome-wide survey in the rat angioplasty model, we studied BRD4 and EZH2 functional regulations involved in IH.We performed chromatin immunoprecipitation sequencing (ChIPseq) using rat carotid arteries. While H3K27me3 ChIPseq signal prevalently intensified in balloon-injured (vs uninjured) arteries, BRD4 and H3K27ac became more enriched at Ezh2. Indeed, BRD4-siRNA or CRISPR-deletion of BRD4-associated enhancer abated the smooth muscle cell (SMC) expression of EZH2, and SMC-specific BRD4 knockout in BRD4fl/fl; Myh11CreERT2 mice reduced both H3K27me3 and IH in wire-injured femoral arteries. In accordance, post-angioplasty IH was exacerbated and mitigated, respectively, by lentiviral expression and pharmacological inhibition of EZH2/1; EZH2 (or EZH1) loss- and gain-of-function respectively attenuated and aggravated pro-IH SMC proliferative behaviors. Furthermore, while H3K27me3 ChIPseq signal magnified at P57 and ebbed at Ccnd1 and Uhrf1 after injury, silencing either EZH2 or EZH1 in SMCs up-regulated P57 and down-regulated Ccnd1 and Uhrf1.In summary, our results reveal an upsurge of EZH2/H3K27me3 after angioplasty, BRD4’s control over EZH2 expression, and non-redundant EZH2/1 functions. As such, this study unravels angioplasty-induced loci-specific H3K27me3/ac redistribution in the epigenomic landscape rationalizing BRD4/EZH2-governed pro-IH regulations.

scholarly journals Genome-Wide Chromatin Immunoprecipitation Sequencing Analysis Shows that WhiB Is a Transcription Factor That Cocontrols Its Regulon with WhiA To Initiate Developmental Cell Division inStreptomyces

mBio ◽  
2016 ◽  
Vol 7 (2) ◽  
Author(s):  
Matthew J. Bush ◽  
Govind Chandra ◽  
Maureen J. Bibb ◽  
Kim C. Findlay ◽  
Mark J. Buttner
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Dna Binding ◽  
Chromatin Immunoprecipitation ◽  
Sequencing Analysis ◽  
Founding Member ◽  
Genome Wide ◽  
Biochemical Function ◽  
Chromatin Immunoprecipitation Sequencing

ABSTRACTWhiB is the founding member of a family of proteins (theWhiB-like [Wbl] family) that carry a [4Fe-4S] iron-sulfur cluster and play key roles in diverse aspects of the biology of actinomycetes, including pathogenesis, antibiotic resistance, and the control of development. InStreptomyces, WhiB is essential for the process of developmentally controlled cell division that leads to sporulation. The biochemical function of Wbl proteins has been controversial; here, we set out to determine unambiguously if WhiB functions as a transcription factor using chromatin immunoprecipitation sequencing (ChIP-seq) inStreptomyces venezuelae. In the first demonstration ofin vivogenome-wide Wbl binding, we showed that WhiB regulates the expression of key genes required for sporulation by binding upstream of ~240 transcription units. Strikingly, the WhiB regulon is identical to the previously characterized WhiA regulon, providing an explanation for the identical phenotypes ofwhiAandwhiBmutants. Using ChIP-seq, we demonstrated thatin vivoDNA binding by WhiA depends on WhiB and vice versa, showing that WhiA and WhiB function cooperatively to control expression of a common set of WhiAB target genes. Finally, we show that mutation of the cysteine residues that coordinate the [4Fe-4S] cluster in WhiB prevents DNA binding by both WhiB and WhiAin vivo.IMPORTANCEDespite the central importance ofWhiB-like (Wbl) proteins in actinomycete biology, a conclusive demonstration of their biochemical function has been elusive, and they have been difficult to study, particularlyin vitro, largely because they carry an oxygen-sensitive [4Fe-4S] cluster. Here we used genome-wide ChIP-seq to investigate the function ofStreptomycesWhiB, the founding member of the Wbl family. The advantage of this approach is that the oxygen sensitivity of the [4Fe-4S] cluster becomes irrelevant once the protein has been cross-linked to DNAin vivo. Our data provide the most compellingin vivoevidence to date that WhiB, and, by extension, probably all Wbl proteins, function as transcription factors. Further, we show that WhiB does not act independently but rather coregulates its regulon of sporulation genes with a partner transcription factor, WhiA.

scholarly journals Identification of Transcribed Enhancers by Genome-Wide Chromatin Immunoprecipitation Sequencing

2016 ◽  
pp. 91-109 ◽  
Author(s):  
Steven Blinka ◽  
Michael H. Reimer ◽  
Kirthi Pulakanti ◽  
Luca Pinello ◽  
Guo-Cheng Yuan ◽  
...  
Keyword(s):  
Chromatin Immunoprecipitation ◽  
Genome Wide ◽  
Chromatin Immunoprecipitation Sequencing
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