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Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26685 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA136591

REPOSITORIES: GEO

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Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-01 | E-GEOD-26685 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [expression]

Project description:Genome wide gene expression profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The sample treated with non target siRNA and PBS serves as control sample. Total RNA obtained from isolated RKO cells.

2013-01-01 | E-GEOD-26684 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [Methylation]

Project description:Genome wide DNA methylation profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across 27,578 CpGs in treated RKO cells. Samples included cells under 4 different treatments. The sample treated with non target siRNA and PBS serves as control sample. Bisulphite converted DNA from the 4 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2013-01-01 | E-GEOD-26433 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [Methylation]

2013-01-01 | GSE26433 | GEO

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [expression]

2013-01-01 | GSE26684 | GEO

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

Project description:Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

| PRJNA136591 | ENA

Gene reactivation by 5-aza-2'-deoxycytidine-induced demethylation requires SRCAP-mediated H2A.Z insertion to establish nucleosome depleted regions.

Project description:5-Aza-2'-deoxycytidine, approved by the FDA for the treatment of myelodysplastic syndrome (MDS), is incorporated into the DNA of dividing cells where it specifically inhibits DNA methylation by forming covalent complexes with the DNA methyltransferases (DNMTs). In an effort to study the correlations between DNA methylation, nucleosome remodeling, and gene reactivation, we investigate the integrated epigenetic events that worked coordinately to reprogram the methylated and closed promoters back to permissive chromatin configurations after 5-Aza-2'-deoxycytidine treatment. The ChIP results indicate that H2A.Z is deposited at promoter regions by the Snf2-related CBP activator protein (SRCAP) complex following DNA demethylation. According to our genome-wide expression and DNA methylation profiles, we find that the complete re-activation of silenced genes requires the insertion of the histone variant H2A.Z, which facilitates the acquisition of regions fully depleted of nucleosome as demonstrated by NOMe-seq (Nucleosome Occupancy Methylome-sequencing) assay. In contrast, SRCAP-mediated H2A.Z deposition is not required for maintaining the active status of constitutively expressed genes. By combining Hpa II digestion with NOMe-seq assay, we show that hemimethylated DNA, which is generated following drug incorporation, remains occupied by nucleosomes. Our data highlight H2A.Z as a novel and essential factor involved in 5-Aza-2'-deoxycytidine-induced gene reactivation. Furthermore, we elucidate that chromatin remodeling translates the demethylation ability of DNMT inhibitors to their downstream efficacies, suggesting future therapeutic implications for chromatin remodelers.

| S-EPMC3315468 | biostudies-literature

Essential role of p18Hamlet/SRCAP-mediated histone H2A.Z chromatin incorporation in muscle differentiation.

Project description:The chromatin-remodelling complex SNF2-related CBP activator protein (SRCAP) regulates chromatin structure in yeast by modulating the exchange of histone H2A for the H2A.Z variant. Here, we have investigated the contribution of H2A.Z-mediated chromatin remodelling to mammalian cell differentiation reprogramming. We show that the SRCAP subunit named ZNHIT1 or p18(Hamlet), which is a substrate of p38 MAPK, is recruited to the myogenin promoter at the onset of muscle differentiation, in a p38 MAPK-dependent manner. We also show that p18(Hamlet) is required for H2A.Z accumulation into this genomic region and for subsequent muscle gene transcriptional activation. Accordingly, downregulation of several subunits or the SRCAP complex impairs muscle gene expression. These results identify SRCAP/H2A.Z-mediated chromatin remodelling as a key early event in muscle differentiation-specific gene expression. We also propose a mechanism by which p38 MAPK-mediated signals are converted into chromatin structural changes, thereby facilitating transcriptional activation during mammalian cell differentiation.

| S-EPMC2892367 | biostudies-literature

MicroRNA-939 restricts Hepatitis B virus by targeting Jmjd3-mediated and C/EBPα-coordinated chromatin remodeling.

Project description:Multi-layered mechanisms of virus host interaction exist for chronic hepatitis B virus (HBV) infection, which have been typically manifested at the microRNA level. Our previous study suggested that miRNA-939 (miR-939) may play a potential role in regulating HBV replication. Here we further investigated the mechanism by which miR-939 regulates HBV life cycle. We found that miR-939 inhibited the abundance of viral RNAs without direct miRNA-mRNA base pairing, but via host factors. Expression profiling and functional validation identified Jmjd3 as a target responsible for miR-939 induced anti-HBV effect. Jmjd3 appeared to enhance the transcription efficiency of HBV enhancer II/core promoter (En II) in a C/EBPα-dependent manner. However, the demethylase activity of Jmjd3 was not required in this process. Rather, Jmjd3's transactivation activity depended on its interaction with C/EBPα. This coordinated action further recruited the Brm containing SWI/SNF chromatin remodeling complex which promoted the transcription of HBV RNAs. Taken together, we propose that the miR-939-Jmjd3 axis perturbs the accessibility of En II promoter to essential nuclear factors (C/EBPα and SWI/SNF complex) therefore leading to compromised viral RNA synthesis and hence restricted viral multiplication.

| S-EPMC5078794 | biostudies-literature

TIP48/Reptin and H2A.Z requirement for initiating chromatin remodeling in estrogen-activated transcription.

Project description:Histone variants, including histone H2A.Z, are incorporated into specific genomic sites and participate in transcription regulation. The role of H2A.Z at these sites remains poorly characterized. Our study investigates changes in the chromatin environment at the Cyclin D1 gene (CCND1) during transcriptional initiation in response to estradiol in estrogen receptor positive mammary tumour cells. We show that H2A.Z is present at the transcription start-site and downstream enhancer sequences of CCND1 when the gene is poorly transcribed. Stimulation of CCND1 expression required release of H2A.Z concomitantly from both these DNA elements. The AAA+ family members TIP48/reptin and the histone variant H2A.Z are required to remodel the chromatin environment at CCND1 as a prerequisite for binding of the estrogen receptor (ER?) in the presence of hormone. TIP48 promotes acetylation and exchange of H2A.Z, which triggers a dissociation of the CCND1 3' enhancer from the promoter, thereby releasing a repressive intragenic loop. This release then enables the estrogen receptor to bind to the CCND1 promoter. Our findings provide new insight into the priming of chromatin required for transcription factor access to their target sequence. Dynamic release of gene loops could be a rapid means to remodel chromatin and to stimulate transcription in response to hormones.

| S-EPMC3630088 | biostudies-literature

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