The repressive role of H2A.Z variant in transcriptional regulation depends on AtBMI1 activity in Arabidopsis
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ABSTRACT:
PROVIDER: PRJNA483876 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7631570_1.fastq.gz | Fastqsanger.gz | |||
| SRR7631570_2.fastq.gz | Fastqsanger.gz | |||
| SRR7631571_1.fastq.gz | Fastqsanger.gz | |||
| SRR7631571_2.fastq.gz | Fastqsanger.gz | |||
| SRR7631572_1.fastq.gz | Fastqsanger.gz |
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Project description:H2A.Z variant has emerged as a critical player in regulating plant responses to environment; however, the mechanism by which H2A.Z mediates this regulation remains unclear. In Arabidopsis, H2A.Z has been proposed to have opposite effects on transcription depending on its localization within the gene. These opposite roles have been assigned by correlating gene expression and H2A.Z enrichment analyses but without considering the impact of possible H2A.Z posttranslational modifications. Here we show that H2A.Z can be monoubiquitinated by the PRC1 components AtBMI1A/B/C. The incorporation of this modification is required for H2A.Z-mediated transcriptional repression through a mechanism that does not require PRC2 activity. Our data suggest that the dual role of H2A.Z in regulating gene expression depends on the modification that it carries, while the levels of H2A.Z within genes depend on the transcriptional activity.
2019-05-24 | GSE117969 | GEO
Project description:Gene regulatory programs in different cell types are largely defined through cell-specific enhancers activity. The histone variant H2A.Z has been shown to play important roles in transcription mainly by controlling proximal promoters, but its effect on enhancer functions remains unclear. Here, we demonstrate by genome-wide approaches that H2A.Z is present at a subset of active enhancers bound by the estrogen receptor alpha (ERα). We also determine that H2A.Z does not influence the local nucleosome positioning around ERα-enhancers using ChIP-sequencing at nucleosomal resolution and unsupervised pattern discovery. We further highlight that H2A.Z-enriched enhancers are associated with chromatin accessibility, H3K122ac enrichment and hypomethylated DNA. Moreover, upon estrogen stimulation, the enhancers occupied by H2A.Z produce enhancer RNAs (eRNAs), and recruit RNA polymerase II as well as RAD21, a member of the cohesin complex involved in chromatin interactions between enhancers and promoters. Importantly, their recruitment and eRNAs production are abolished by H2A.Z depletion, thereby revealing a novel functional link between H2A.Z occupancy and enhancer activity. Taken together, our findings suggest that H2A.Z acts as an important player for enhancer functions by establishing and maintaining a chromatin environment required for RNA polymerase II recruitment, eRNAs transcription and enhancer-promoters interactions, all essential attributes of enhancer activity. The MNase ChIP-seqs in this study measure the genome-wide binding landscape of H2A.Z, H3K4me1, H3K27ac and H3K4me3 in MCF-7 cells in the absence or presence of E2. Two biological replicates were done for each ChIP-seq experiment and for each condition, as well as, control input.
2015-08-31 | E-GEOD-57436 | biostudies-arrayexpress
Project description:H2A.Z variant has emerged as a critical player in regulating plant responses to environment; however, the mechanism by which H2A.Z mediates this regulation remains unclear. In Arabidopsis, H2A.Z has been proposed to have opposite effects on transcription depending on its localization within the gene. These opposite roles have been assigned by correlating gene expression and H2A.Z enrichment analyses but without considering the impact of possible H2A.Z post-translational modifications. Here, we show that H2A.Z can be monoubiquitinated by the PRC1 components AtBMI1A/B/C. The incorporation of this modification is required for H2A.Z-mediated transcriptional repression through a mechanism that does not require PRC2 activity. Our data suggest that the dual role of H2A.Z in regulating gene expression depends on the modification that it carries, while the levels of H2A.Z within genes depend on the transcriptional activity.
| S-EPMC6597585 | biostudies-literature
Project description:The incorporation of histone variant H2A.Z, a conserved H2A variant, into nucleosomes creates specialized chromatin domains that regulate DNA-templated processes, including transcription. H2A.Z-containing nucleosomes may poise gene regulatory regions for transcription, but mechanistic details are lacking. In Saccharomyces cerevisiae, the diverging H2A.Z C-terminus is thought to provide the H2A.Z exclusive functions. To elucidate the roles of this H2A.Z C-terminus genome wide, we made use of derivatives where the C-terminus was replaced with the corresponding region of H2A (ZA protein), or the H2A region plus a transcriptional activating peptide, with the idea of regenerating the H2A.Z-dependent regulation globally. An assessment of the genome-wide distribution of these H2A.Z derivatives shows that the H2A.Z C-terminal region is crucial for both maintaining the occupation level of H2A.Z and the proper positioning of the targeted nucleosomes. Interestingly, the specific contribution on incorporation efficiency vs nucleosome positioning varies enormously, depending on loci analyzed. For the ZA protein, positioning changes most importantly near origins of replication and snoRNA gene promoters, while incorporation is affected on all other sites. Furthermore, the role of H2A.Z in global transcription regulation also depends on its C-terminal region. Remarkably however, the latter mostly involves genes without a H2A.Z nucleosome in the promoter.
2022-08-18 | GSE156492 | GEO
Project description:Gene regulatory programs in different cell types are largely defined through cell-specific enhancers activity. The histone variant H2A.Z has been shown to play important roles in transcription mainly by controlling proximal promoters, but its effect on enhancer functions remains unclear. Here, we demonstrate by genome-wide approaches that H2A.Z is present at a subset of active enhancers bound by the estrogen receptor alpha (ERα). We also determine that H2A.Z does not influence the local nucleosome positioning around ERα-enhancers using ChIP-sequencing at nucleosomal resolution and unsupervised pattern discovery. We further highlight that H2A.Z-enriched enhancers are associated with chromatin accessibility, H3K122ac enrichment and hypomethylated DNA. Moreover, upon estrogen stimulation, the enhancers occupied by H2A.Z produce enhancer RNAs (eRNAs), and recruit RNA polymerase II as well as RAD21, a member of the cohesin complex involved in chromatin interactions between enhancers and promoters. Importantly, their recruitment and eRNAs production are abolished by H2A.Z depletion, thereby revealing a novel functional link between H2A.Z occupancy and enhancer activity. Taken together, our findings suggest that H2A.Z acts as an important player for enhancer functions by establishing and maintaining a chromatin environment required for RNA polymerase II recruitment, eRNAs transcription and enhancer-promoters interactions, all essential attributes of enhancer activity.
2015-08-31 | GSE57436 | GEO
Project description:Chromatin modifications have been implicated in the self-renewal and differentiation of embryonic stem cells (ESCs). However, the function of histone variant H2A.Z in ESCs remains unclear. We show that H2A.Z is highly enriched at promoters and enhancers and is required for both efficient self-renewal and differentiation of murine ESCs. H2A.Z deposition leads to an abnormal nucleosome structure, decreased nucleosome occupancy and increased chromatin accessibility. In self-renewing ESCs, knockdown of H2A.Z compromises OCT4 binding to its target genes and leads to decreased binding of MLL complexes to active genes and of PRC2 complex to repressed genes in self-renewal of ESCs. During differentiation of ESCs, inhibition of H2A.Z also compromises RA-induced RARα binding, activation of differentiation markers and the repression of pluripotency genes. We propose that H2A.Z mediates such contrasting activities by acting as a 'general facilitator' that generates access for a variety of complexes both activating and repressive. ChIP-Seq in murine embryonic stem (mES) cells for H2A.Z and acetylated H2A.Z. ChIP-Seq of H3K4me3, H3K27me3, RbBP5, SUZ12 and OCT4 for mES cells of both H2A.Z RNAi knockdown and shLuc control. ChIP-Seq of RARalpha in H2A.Z knockdown (withdraw of LIF and exposure to RA for 3h) and control cells. MNase-Seq and chromatin accessibility assay using Benzonase digestion followed by next-generation sequencing for mES cells of both H2A.Z RNAi knockdown and shLuc control. ChIP-Seq of H2A.Z and H3K4me3 for mES cells of both MLL4 RNAi knockdown and shLuc control. RNA-Seq for mES cells of H2A.Z knockdown and shluc control. RNA-Seq for embryonic bodies derived from mES cells (H2A.Z knockdown and shLuc control) at day 3 and day 7.
2012-12-20 | E-GEOD-34483 | biostudies-arrayexpress
Project description:Here we report a novel role for H2A.Z.2 (H2AFV) as a mediator of cell proliferation and sensitivity to targeted therapies in malignant melanoma. While both H2A.Z.1 and H2A.Z.2 are highly expressed in metastatic melanoma and correlate with decreased patient survival, only H2A.Z.2 deficiency results in impaired cellular proliferation of melanoma cells, which occurs via a G1/S arrest. Integrated gene expression and ChIP-seq analyses revealed that H2A.Z.2 positively regulates E2F target genes, and that such genes acquire a distinct H2A.Z occupancy signature over the promoter and gene body in metastatic melanoma cells. We further identified the BET family member BRD2 as an H2A.Z-interacting protein in melanoma cells, and demonstrate that H2A.Z.2 silencing cooperates with BET inhibition to induce cell death. Total RNA samples from SKmel147 melanoma cell line. Transcript levels were analyzed after control or H2AZ variant RNA interference.
2015-07-01 | E-GEOD-59026 | biostudies-arrayexpress
Project description:Chromatin modifications have been implicated in the self-renewal and differentiation of embryonic stem cells (ESCs). However, the function of histone variant H2A.Z in ESCs remains unclear. We show that H2A.Z is highly enriched at promoters and enhancers and is required for both efficient self-renewal and differentiation of murine ESCs. H2A.Z deposition leads to an abnormal nucleosome structure, decreased nucleosome occupancy and increased chromatin accessibility. In self-renewing ESCs, knockdown of H2A.Z compromises OCT4 binding to its target genes and leads to decreased binding of MLL complexes to active genes and of PRC2 complex to repressed genes in self-renewal of ESCs. During differentiation of ESCs, inhibition of H2A.Z also compromises RA-induced RARα binding, activation of differentiation markers and the repression of pluripotency genes. We propose that H2A.Z mediates such contrasting activities by acting as a 'general facilitator' that generates access for a variety of complexes both activating and repressive.
2012-12-20 | GSE34483 | GEO
Project description:Histone variant H2A.Z regulates zygotic genome activation
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Project description:Nucleosome is the basic structural unit of chromatin, and its dynamics plays critical roles in the regulation of genome functions. However, how the nucleosome structure is regulated by histone variants in vivo is still largely uncharacterized. Here, by employing Micrococcal nuclease (MNase) digestion of crosslinked chromatin followed by chromatin immunoprecipitation (ChIP) and paired-end sequencing (MNase-X-ChIP-seq), we mapped genome-wide unwrapping states of nucleosomes containing histone variant H2A.Z in mouse embryonic stem (ES) cells. We found that H2A.Z is enriched with unwrapped nucleosomes. Interestingly, the function of +1 H2A.Z nucleosome in transcriptional regulation is correlated with the unwrapping states. We further showed that H2A.Z nucleosomes adjacent the CTCF binding sites (CBS) may adopt an open conformation. We confirmed the unwrapping state of H2A.Z nucleosomes under native condition by re-ChIP of H2A.Z after CTCF CUT&RUN in mouse ES cells. Importantly, we found that depletion of H2A.Z results in increased CTCF binding, indicating dynamic competition between the unwrapped H2A.Z nucleosomal intermediates and CTCF at the CBS. Taken together, our results showed that histone variant H2A.Z regulates transcription and CTCF binding through modulating the nucleosome unwrapping.
2020-04-27 | GSE146082 | GEO