Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H2AK121ub and H3K27me3 marks have different effects on nucleosome organization in Arabidopsis

ABSTRACT: Background: Nucleosome organization within chromatin can be altered through the incorporation of histone modifications that in turn affects gene expression. Accordingly, the Polycomb Group (PcG) complexes PRC1 and PRC2 through the incorporation of H2AK121ub and H3K27me3 marks, respectively, maintain the repression of target genes; however, little is known about the exact function of these modifications in shaping nucleosome array at target genes, especially in plants. Results: By using two different MNase-seq datasets we analyzed the nucleosome occupancy profile of different PcG target genes in Arabidopsis. We found that PcG targets strongly differ in their nucleosome organization depending on the marks that they carry. Our data indicate that H2AK121ub marks play a role in fine-tuning +1 nucleosome position, while H3K27me3 marks impact nucleosome spacing and chromatin accessibility at both promoter and gene regions. Furthermore, analyzing the nucleosome profile of transcriptionally active PcG target genes in WT seedlings we found that their apparent activated state may be actually due to transcriptional heterogeneity across different cells. Conclusion: Our findings show that H2AK121ub and H3K27me3 marks differentially affect nucleosome organization in Arabidopsis, displaying additive effects when co-localizing at target genes.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE135978 | GEO | 2022/02/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

H2AK121ub in Arabidopsis favors a less accessible chromatin state at transcriptional regulation hotspots [RNA-seq]

Project description:Although it is well established that Polycomb Group (PcG) complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3, little is known about the effect of these modifications on chromatin, which is fundamental to understand PcG function. Here, by integrating chromatin accessibility, histone marks and expression analyses in different Arabidopsis PcG mutants, we show that H2AK121ub marking favors a less accessible but still permissive chromatin at transcriptional regulation hotspots, which can be further reduced by EMF1 and H3K27me3. We found that when acting concurrently, H2AK121ub and H3K27me3 establish an inaccessible but responsive chromatin to marks levels, allowing gene reprograming. Conversely, when H3K27me3 is alone, chromatin is less responsive, indicating that H2AK121ub-marked hotspots are required for transcriptional responses. Interestingly, despite the loss of H2AK121ub and H3K27me3 leads to increased chromatin accessibility, this is not necessarily accompanied by transcriptional activation, indicating that gene expression is not always predictive of accessible chromatin.

2020-12-02 | GSE154697 | GEO

H2AK121ub in Arabidopsis favors a less accessible chromatin state at transcriptional regulation hotspots [ChIP-seq]

2020-12-02 | GSE154696 | GEO

H2AK121ub in Arabidopsis favors a less accessible chromatin state at transcriptional regulation hotspots [ATAC-seq]

2020-12-02 | GSE154695 | GEO

H2AK121ub and H3K27me3 marks have different effects on nucleosome organization in Arabidopsis

Project description:H2AK121ub and H3K27me3 marks have different effects on nucleosome organization in Arabidopsis

| PRJNA560876 | ENA

H2A monoubiquitination in Arabidopsis is generally independent of LHP1 and PRC2 activity [ChIP-seq]

Project description:BACKGROUND: Polycomb group complexes PRC1 and PRC2 repress gene expression at the chromatin level in eukaryotes. The classic recruitment model of Polycomb group complexes in which PRC2-mediated H3K27 trimethylation recruits PRC1 for H2A monoubiquitination was recently challenged by data showing that PRC1 activity can also recruit PRC2. However, the prevalence of these two mechanisms is unknown, especially in plants as H2AK121ub marks were examined at only a handful of Polycomb group targets. RESULTS: By using genome-wide analyses, we show that H2AK121ub marks are surprisingly widespread in Arabidopsis thaliana, often co-localizing with H3K27me3 but also occupying a set of transcriptionally active genes devoid of H3K27me3. Furthermore, by profiling H2AK121ub and H3K27me3 marks in atbmi1a/b/c, clf/swn, and lhp1 mutants we found that PRC2 activity is not required for H2AK121ub marking at most genes. In contrast, loss of AtBMI1 function impacts the incorporation of H3K27me3 marks at most Polycomb group targets. CONCLUSIONS: Our findings show the relationship between H2AK121ub and H3K27me3 marks across the A. thaliana genome and unveil that ubiquitination by PRC1 is largely independent of PRC2 activity in plants, while the inverse is true for H3K27 trimethylation.

2017-03-21 | GSE89357 | GEO

H2A monoubiquitination in Arabidopsis is generally independent of LHP1 and PRC2 activity [RNA-seq]

2017-03-21 | GSE89356 | GEO

The domesticated transposase ALP2 mediates formation of a novel Polycomb protein complex by direct interaction with MSI1, a core subunit of Polycomb Repressive Complex 2 (PRC2)

Project description:A large fraction of plant genomes is composed of transposable elements (TE), which provide a potential source of novel genes through “domestication” – the process whereby the proteins encoded by TE diverge in sequence, lose their ability to catalyse transposition and instead acquire novel functions for their hosts. In Arabidopsis, ANTAGONIST OF LIKE HETEROCHROMATIN PROTEIN 1 (ALP1) arose by domestication of the nuclease component of Harbinger class TE and acquired a new function as a component of POLYCOMB REPRESSIVE COMPLEX 2 (PRC2), a histone H3K27me3 methyltransferase involved in regulation of host genes and in some cases TE. It was not clear how ALP1 associated with PRC2, nor what the functional consequence was. Here, we identify ALP2 genetically as a suppressor of Polycomb-group (PcG) mutant phenotypes and show that it arose from the second, DNA binding component of Harbinger transposases. Molecular analysis of PcG compromised backgrounds reveals that ALP genes oppose silencing and H3K27me3 deposition at key PcG target genes. Proteomic analysis reveals that ALP1 and ALP2 are components of a variant PRC2 complex that contains the four core components but lacks plant-specific accessory components such as the H3K27me3 reader LIKE HETEROCHROMATION PROTEIN 1 (LHP1). We show that the N-terminus of ALP2 interacts directly with ALP1, whereas the C-terminus of ALP2 interacts with MULTICOPY SUPPRESSOR OF IRA1 (MSI1), a core component of PRC2. Proteomic analysis reveals that in alp2 mutant backgrounds ALP1 protein no longer associates with PRC2, consistent with a role for ALP2 in recruitment of ALP1. We suggest that the propensity of Harbinger TE to insert in gene-rich regions of the genome, together with the modular two component nature of their transposases, has predisposed them for domestication and incorporation into chromatin modifying complexes.

2020-05-18 | PXD018911 | Pride

SAM domain polymerization links subnuclear clustering of PRC1 to silencing

Project description:Polycomb group (PcG) proteins mediate heritable but reversible silencing of developmental regulator genes by modifying their chromatin configuration. Accumulating evidence documents a role for PcG proteins in regulating higher order chromatin structures likely by their clustering, however, underlying mechanisms and its impact on transcriptional regulation remain obscure. In this study, we found that subnuclear clustering of PRC1 at canonical PcG target genes depended on head-to-tail polymerization property of SAM domain of Phc2 and likely Phc1. We show that Phc2-SAM polymerization limits the dynamic nature of PRC1, thereby promotes stable association of PRC1 with PcG target genes and contributes to their robust silencing. Our findings suggest a novel model by which SAM polymerization of Phc2 modulates the structural organization of PcG complexes to enable robust yet reversible PcG-mediated repression during development. Examination of H3K27me3 in wild type and the Phc2 mutant cells

2013-06-01 | E-GEOD-37530 | biostudies-arrayexpress

GFI1 tethers the NuRD complex to open and transcriptionally active chromatin in myeloid progenitors

Project description:GFI is a DNA binding transcriptional repressor that regulates myeloid differentiation. Here, we show that GFI1 interacts with the chromodomain helicase CHD4 and other components of the nucleosome remodeling and deacetylase (NuRD) complex. Our data demonstrated that GFI1 and GFI1/CHD4 complexes occupy sites of open chromatin enriched for histone marks associated with active transcription or different sets of genes that are either enriched for IRF1 or SPI-1 consensus binding sites. In addition, our study provided evidence that GFI1 affects the chromatin remodeling activity of the NuRD complex. Overall, our results indicate that GFI1/CHD4 complexes control chromatin openness and histone modifications differentially to regulate target genes, which govern the immune response, nucleosome organization, or metabolic processes.

2021-11-02 | PXD028945 | Pride

Global changes of H3K27me3 domains and PcG protein distribution in the absence of the PcG recruiters Spps or Pho

Project description:Polycomb group (PcG) proteins maintain the silenced state of key developmental genes in animals, but how these proteins are recruited to specific regions of the genome is still poorly understood. In Drosophila, PcG proteins are recruited to Polycomb response elements (PREs) that include combinations of sites for sequence specific DNA binding “PcG recruiters,” including Pho, Cg, and Spps. To understand their roles in PcG recruitment, we compared Pho-, Cg-, and Spps-binding sites against H3K27me3 and key PcG proteins by ChIP-seq in wild-type and mutant third instar larvae. H3K27me3 in canonical Polycomb domains is decreased after the reduction of any recruiter. Reduction of Spps and Pho, but not Cg, causes the redistribution of H3K27me3 to heterochromatin. Regions with dramatically depleted H3K27me3 after Spps knockout are usually accompanied by decreased Pho binding, suggesting their cooperative binding. PcG recruiters, the PRC2 component E(z), and the PRC1 components Psc and Ph cobind thousands of active genes outside of H3K27me3 domains. This study demonstrates the importance of distinct PcG recruiters for the establishment of unique Polycomb domains. Different PcG recruiters can act both cooperatively and independently at specific PcG target genes, highlighting the complexity and diversity of PcG recruitment mechanisms.

2018-03-07 | GSE102339 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data