Dataset Information

Genome-wide profiling of H3K4me3 and H3K27me3 modifications during and after vernalization in Brachypodium

ABSTRACT: Vernalization, the requirement of long-term exposure to low environmental temperature for flowering, is a typical epigenetic phenomenon in plants. Histone modifications have been analyzed for key vernalization genes, but genome-wide regulation remains unclear. Here, we performed global analysis of histone 3 lysine 4 (H3K4me3) and 27 (H3K27me3) trimethylation with Chromatin Immunoprecipitation-Sequencing (ChIP-Seq) during and after vernalization to obtain complete view of histone modification fluctuation both on whole genome scale and for single genes, even different regions of genes. The critical role of H3K27me3 was revealed. During vernalization H3K27me3 regulation concentrated on a few biological processes, with two essential environmental responses, transcription regulation and anti-stress reactions, being main targets, as indicated by change pattern and GO analysis. The regulation of H3K4me3, however, showed no obvious focus. For gene expression, H3K27me3 is involved in multiple trends of control. H3K4me3, however, mainly focuses on unidirectional regulation. After vernalization most of H3K27me3 changes were kept, but relatively small proportion of H3K4me3 changes could be maintained, as shown by multiple-level analysis, suggesting the active role of H3K27me3 in epigenetic memory. Vernalization-induced histone modification changes were uncovered for VRN3, a gene integrating vernalization/photoperiod signals, suggesting its regulation role at epigenetic level. Memory-related genes were genome-widely identified and a high proportion of them showed quantitative response to vernalization-treatment, suggesting broad existence of this mechanism. Our studies shed new light on epigenetic role of H3K27me3 and VRN3 in vernalization, revealed mechanism underlying epigenetic memory, which helps us to further understand vernalization, a mechanism with great potential in agriculture.

ORGANISM(S): Brachypodium distachyon

PROVIDER: GSE93140 | GEO | 2018/05/22

REPOSITORIES: GEO

ACCESS DATA

Similar Datasets

Project description:Epigenetic priming factors establish a permissive epigenetic landscape which is not required until a later developmental or physiological time point, temporally uncoupling the presence of these factors with their phenotypic effects. One classic example of epigenetic priming is in the context of bivalent chromatin, found in pluripotent stem cells and early embryos at key developmental gene promoters marked by both activating-associated H3K4me3 and repressive-associated H3K27me3 histone modifications. It is currently unknown how these bivalent domains are targeted, or precisely how they impact on lineage commitment. Here we show that the small heterodimerising non-enzymatic DNA binding proteins Developmental Pluripotency Associated 2 (Dppa2) and 4 (Dppa4) act as epigenetic priming factors to establish bivalency at a subset of developmental genes. Dppa2/4 localise to the +1 nucleosome position of bivalent genes and while they are not required for pluripotency in embryonic stem cells (ESCs), double knockout cells fail to exit pluripotency and to differentiate efficiently, with delays in upregulating bivalently marked lineage genes. Proteomics reveal that Dppa2/4 interact on chromatin with members of the COMPASS and Polycomb complexes important for H3K4me3 and H3K27me3 deposition, respectively. Epigenetic profiling reveals a striking loss of H3K4me3, H3K27me3, and their associated enzymatic machinery at a significant subset of bivalent promoters in Dppa2/4 mutants, in addition to loss of H2A.Z and chromatin accessibility. In wild-type ESCs, these “Dppa2/4-dependent” bivalent promoters are characterised by low H3K4me3 enrichment and breadth, near-absent expression levels and initiating but not elongating RNA polymerase. Notably, Dppa2/4-dependent promoters are less evolutionarily conserved suggesting that they lack additional safeguard measures to maintain bivalency at these genes in the absence of Dppa2/4. Concomitantly with the loss of bivalency, Dppa2/4-dependent bivalent promoters gain DNA methylation and consequently are no longer able to be effectively activated upon ESC differentiation, leading to defects in cell fate acquisition. Our findings reveal a targeting principle for bivalency to developmental gene promoters poising them for future lineage specific gene activation.

Project description:Histone methylations play a major role in regulating the chromatin state and gene expression, yet little is known about their involvement in differential gene expression and function of memory CD8 T cells. Here, we report a genome-wide analysis of two histone H3 methylations (H3K4me3 and H3K27me3) and gene expression in naïve, central (TCM) and effector (TEM) memory CD8 T cells. Analysis of 16,314 annotated genes in CD8 T cell subsets revealed that gene expression were positively correlated with the levels of H3K4me3 and negatively correlated with the levels of H3K27me3 in these gene loci. The correlation between differential H3K4me3 orH3K27me3 levels with gene expressions in memory CD8 T cells displayed four distinct modes: repressive, active, poised, and bivalent, reflecting their complex regulation and different function of these genes. Furthermore, accessible chromatin states of different gene loci were preferentially influenced by different histone modifications as demonstrated here high levels of H3K9ac found in active gene loci without high levels of H3K4me3. These findings reveal a histone methylation based complex regulation of differential gene expression in memory CD8 T cells. Thus, change of chromatin structure mediated by histone methylation may serve a fundamental basis for the rapid transcriptional response of memory CD8 T cells. Keywords: Histone methylations, chromatin state, CD8 memory T cells Enriched naïve and memory CD8 T cells were purified into CD8+CD45RA+CD62L+ naïve T cells, CD8+CD45RA-CD62L+ central memory T cells (TCM), and CD8+CD45RA-CD62L- effector memory T cells (TEM) by a cell sorter (MoFlo; Dako Cytomation, Carpentaria, CA). Triplicates of each cell type were either used right away or incubated with anti-CD3 and anti-CD28 Ab (anti-CD3/CD28) coupled magnetic beads (Invitrogen) at the cell:bead ratio of 1:1 for 16 hours in RPMI-1640 with 10% Fetal bovine serum and penicillin (10 U/ml)/streptomycin (10 ug/ml) (Invitrogen). The freshly isolated and 16 hr stimulated cells from several donors as a pool were used for gene expression microarray analysis. All sample data was normalized to a standard control RNA labeled and hybed along with each sample and all data from the 3 replicates was averaged.

Dataset Information

Genome-wide profiling of H3K4me3 and H3K27me3 modifications during and after vernalization in Brachypodium

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure