Arabidopsis thaliana
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PROVIDER: PRJNA113725 | ENA |
REPOSITORIES: ENA
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Project description:Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome-wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription. We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity.
2017-04-25 | GSE97252 | GEO
Project description:Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription. We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity.
2017-04-24 | GSE97231 | GEO
Project description:In eukaryotes, DNA wraps around histones to form nucleosomes, which are compacted into chromatin. DNA-templated processes, including transcription, require chromatin disassembly and reassembly mediated by histone chaperones. Additionally, distinct histone variants can replace core histones to regulate chromatin structure and function. Although replacement of H2A with the evolutionarily conserved H2A.Z via the SWR1 histone chaperone complex has been extensively studied, in plants little is known about how a reduction of H2A.Z levels can be achieved. Here, we show that NRP proteins cause a decrease of H2A.Z-containing nucleosomes in Arabidopsis under standard growing conditions. nrp1-1 nrp2-2 double mutants show an over-accumulation of H2A.Z genome-wide, especially at heterochromatic regions normally H2A.Z-depleted in wild-type plants. Our work suggests that NRP proteins regulate gene expression by counteracting SWR1, thereby preventing excessive accumulation of H2A.Z.
2020-05-18 | PXD019248 | Pride
Project description:Interplay Between Active Chromatin Marks and RNA-directed DNA Methylation in Arabidopsis thaliana
| PRJNA213000 | ENA
Project description:The eukaryotic genome is divided into regions of heterochromatin and euchromatin. The histone variant H2A.Z specifically localizes at euchromatin and displays a genome-wide anti-correlation with DNA methylation. DNA methylation plays a central role in the epigenetic regulation of many eukaryotic genomes. Active DNA demethylation is critical for controlling the epigenome in plants and mammals. Yet, little is known about how DNA demethylases are recruited to target loci. Here we report that SWR1, a conserved histone H2A.Z deposition complex, regulates DNA demethylation in Arabidopsis thaliana by recruiting the plant DNA demethylase ROS1. A forward genetic screen for anti-silencing mutants identified two SWR1 components, PIE1 and ARP6, as cellular factors required for ROS1-mediated DNA demethylation. We further discovered two bromodomain-containing proteins, the methyl-DNA-binding protein AtMBD9, and NPX1, a plant homolog of ScBDF1 in yeast, as components of the SWR1 complex in Arabidopsis. AtMBD9 and NPX1 function redundantly in preventing DNA hypermethylation and transcriptional gene silencing by recognizing histone acetylation marks established by IDM1, a known regulator of DNA demethylation. We show that IDM1 is required for H2A.Z deposition in many genomic regions targeted for active DNA demethylation. We found that H2A.Z interacts with ROS1 and is required for locus-specific DNA demethylation and antisilencing. Our results reveal a role of H2A.Z in active DNA demethylation, and a mechanism through which DNA demethylases can be recruited to target regions by specific histone acetylation marks.
2019-08-01 | GSE115170 | GEO
Project description:Bioinformatics powered correlative analysis of epigenomic patterns is an effective method to help derive biological hypotheses that can be tested genetically or biochemically. To accommodate the variety and complexity of epigenomic and transcriptomic patterns, ANchored COrrelative Patterns (ANCORP) was developed as a platform to integrate and intuitively visualize a large number of genome-wide profiles. With global profiles of 9 histone modifications mapped by ChIP-seq and a strand-specific RNA-seq dataset, we have applied the ANCORP-genetics pipeline for hypothesis building and testing in order to understand how global transcription may be regulated by epigenetic pathways such as histone modifications. It was found that intragenic antisense RNAs were depleted from genes with strong gene-body H3K36me2 mark and cytosine methylation enrichments but were significantly overrepresented in H3K4me3/H3K27me3 bivalent genes. Moreover, gene body H3K36me2 and DNA methylation anti-correlated with multiple active chromatin marks including H3K4me2/3, H3K9Ac and H3K18Ac. These observations lead us to hypothesize that H3K36me2 and DNA methylation may synergistically repress active chromatin marks in gene bodies and subsequently inhibit transcription of the antisense strand. Mutant analyses revealed that Polymerase Associated Factors (PAF) may be universally required for modulating NAT abundance whereas the role for the 5mC and H3K36me marks are more locus specific. H3K36me and PAF may either repress or permit the accumulation NATs depending on the chromatin state context in a particular transcription unit. Interestingly, the activation of antisense RNA in sdg8-2 or elf8-1 mutants does not associate with any increase of histone marks in gene bodies that are known to correlate with gene activation. Our results suggest that ANCORP-genetics is an effective approach to uncover epigenetic regulatory mechanisms by leveraging on the rapid advances in sequencing technologies and the resultant wealth of genome-wide information.
2011-06-06 | GSE28398 | GEO
Project description:Eukaryotic chromatin is separated into functional domains differentiated by posttranslational histone modifications, histone variants, and DNA methylation. Methylation is associated with repression of transcriptional initiation in plants and animals, and is frequently found in transposable elements. Proper methylation patterns are critical for eukaryotic development, and aberrant methylation-induced silencing of tumor suppressor genes is a common feature of human cancer. In contrast to methylation, the histone variant H2A.Z is preferentially deposited by the Swr1 ATPase complex near 5' ends of genes where it promotes transcriptional competence. How DNA methylation and H2A.Z influence transcription remains largely unknown. Here we show that in the plant Arabidopsis thaliana, regions of DNA methylation are quantitatively deficient in H2A.Z. Exclusion of H2A.Z is seen at sites of DNA methylation in the bodies of actively transcribed genes and in methylated transposons. Mutation of the MET1 DNA methyltransferase, which causes both losses and gains of DNA methylation, engenders opposite changes in H2A.Z deposition, while mutation of the PIE1 subunit of the Swr1 complex that deposits H2A.Z17 leads to genome-wide hypermethylation. Our findings indicate that DNA methylation can influence chromatin structure and effect gene silencing by excluding H2A.Z, and that H2A.Z protects genes from DNA methylation. Keywords: Affinity-purification on microarray All experiments were done using two channels per chip. DNA methylation experiments compared immunoprecipitated, methylated DNA to control genomic DNA. H2A.Z experiments compared whole micrococcal nuclease-treated affinity-purified chromatin to input chromatin used for affinity purification. Affinity purification was performed using either biotin-tagged H2A.Z, pulled down using streptavidin, or endogenous H2A.Z pulled down using an anti-H2A.Z antibody.
2008-10-02 | E-GEOD-12212 | biostudies-arrayexpress
Project description:Chromatin structure and function is maintained by dynamic protein-protein and protein-nucleic acid interactions. Histones are a family of proteins that are abundant chromatin constituents and that carry numerous post-translational modifications (PTMs). Histone PTMs mediate a variety of biological activities, including recruitment of enzymatic readers, writers and erasers that modulate protein activities, DNA replication, transcription and repair. Individual histone molecules contain multiple co-existing PTMs some of which exhibit crosstalk, i.e. coordinated or mutually exclusive activities. We here present an integrated experimental and computational approach for systems level molecular characterization of PTMs and PTM crosstalk. Using wildtype and engineered mouse embryonic stem cells with perturbations in the Polycomb Repressive Complex 1 (PRC1, suz12-/-), PRC2 (Ring1A/b-/-) and DNA methyltransferases (Dnmt1/3a/3b-/-) we performed comprehensive PTM analysis of histone H3 tails. We identified unique histone H3 PTM features of each of the four cell lines and we detected common combinatorial PTM features across cell lines. Using quantitative middle-down proteomics combined with probabilistic and statistical data analysis we extracted histone H3 PTM profiles for all four mESC systems. PTM crosstalk emerged as mutually exclusive histone PTMs or coordinately regulated PTMs independent of histone peptide abundance in the four model systems. We detected positive crosstalk between adjacent mono-methylated marks but strong negative crosstalk among most of the seven characterized di- and tri-methylations on lysines. We report novel features of PTM interplay involving hitherto poorly characterized arginine methylation and lysine methylation sites in histone H3, including H3R2me, H3R8me and H3K37me, which exhibited specific PTM codes suggesting a particular role in chromatin. All histone H3 PTM data is available in our publicly available CrossTalkDB repository at http://crosstalkdb.bmb.sdu.dk
2016-06-16 | PXD002560 | Pride
Project description:Epigenetic states defined by chromatin can be maintained through mitotic cell division. However, it remains unknown how histone-based information is transmitted. Here we combine nascent chromatin capture (NCC) and triple-SILAC labelling to track histone modifications and histone variants during DNA replication and across the cell cycle. We show that post-translational modifications (PTMs) are transmitted with parental histones to newly replicated DNA. Di- and tri-methylation marks are diluted two-fold upon DNA replication, as a consequence of new histone deposition. Importantly, within one cell cycle all PTMs are restored. In general, new histones are modified to mirror the parental histones. However, H3K9me3 and H3K27me3 are propagated by continuous modification of parental and new histones, because the establishment of these marks extends over several cell generations. Together, our results reveal how histone marks propagate and demonstrate that chromatin states oscillate within the cell cycle.
2015-03-30 | PXD001980 | Pride
Project description:We report the survey of two repressive epigenetic marks in hand-dissected mature Arabidopsis embryos. DNA from approximately 2500 embryos was extracted for each samples. DNA was treated with bisulfite and fractionated for whole genome bisulfite sequencing to reveal methylated cytosines. Chromatin was fractionnated and immuno-precipited with either anti-H3K9me2 or anti-H3 to test for histone methylation. Both profiles were compared in different mutant backgrounds to survey how small RNA influence reprogramming in the embryo.
2021-05-26 | GSE147245 | GEO