Chromatin state for BS and M cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Zea mays
PROVIDER: GSE206002 | GEO | 2022/08/03
REPOSITORIES: GEO
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Project description:The model describing that aberrant CpG island (CGI) methylation leads to transcription repression of tumor suppressor genes and thereby is implicated in tumor progression has been established in many cancers. However, recent studies indicated aberrantly hypermethylated genes in multiple cancers are already repressed in pre-cancerous tissues despite their promoters are hypomethylated. Here, we hypothesized that the occurrence of CGI promoter hypermethylation in cancers are associated with Polycomb-repressive complex and the associated H3K27me3 mark in pre-cancerous tissues. By using a ChIP-BS-seq technology that examines methylation of the DNA fragments precipitated by the antibodies to histone modifications, we provided direct evidences showing that genes highly enriched with H3K27me3 marks both in cancer and normal cells became aberrantly hypermethylated in CGI promoters in cancer cells in comparison with normal cells. Furthermore, we confirmed that these genes consistently were significantly hypermethylated in TCGA primary cancer in comparison with normal tissues. Thus, we provided direct evidences supporting that the presence of H3K27m3 may serve as a guide to promoter hypermethylation. This will spur future work on epigenetic signature of combined histone and DNA methylation that could define a cancerM-bM-^@M-^Ys epigenetic abnormalities, therefore helping distinguish subtypes of cancers and aiding future diagnosis and therapeutics of cancers. We applied ChIP-BS technology to examine H3K27me3 marks, which are catalyzed by the SET domain histone methyltransferase EZH2 and have a repressive function with 50bp pair-end sequencing. found H3K27me3 marks were enriched preferentially at CpG islands, (+/-500) transcription start sites (TSSs) and exons in two GC cell lines (BGC-823 and AGS). In YH cells, H3K27me3 marks were only preferentially enriched at CpG islands. In contrast, Hela cells presented a reverse pattern with highest H3K27me3 enrichment in intergenic regions. To confirm this result in Hela cells, we performed two independent replicates of ChIP-Seq and ChIP-BS-seq. Cause of useful was relative small. we still sequenced one 100bp pe reads replicate for H3K4me3 and two replicate for H3K27me3 ChIP-BS-seq.
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Project description:In eukaryotic cells, DNA is tightly packed in the nucleus in chromatin which has histones as its main protein component. Histones are subject to a large number of distinct post-translational modifications, whose sequential or combinatorial action affects genome function. Here, we report the identification of acetylation at lysine 36 in histone H3 (H3K36ac) as a modification in Arabidopsis thaliana. H3K36ac was found to be an evolutionary conserved modification in seed plants. It is highly enriched in euchromatin and very low in heterochromatin. Genome-wide ChIP-seq experiments revealed that H3K36ac is generally found at the 5â?? end of genes. Independently of gene length, H3K36ac covers about 500 bp, about two to three nucleosomes, immediately downstream of the transcriptional start. H3K36ac overlaps with H3K4me3 and the H2A.Z histone variant. The histone acetyl transferase GCN5 and the histone deacetylase HDA19 are required for normal steady state levels of H3K36ac in plants. There is negative crosstalk between H3K36ac and H3K36me3, mediated by the histone methyl transferase SDG8 and GCN5. H3K36ac levels are associated with transcriptional activity but show no linear relation. Instead, H3K36ac is a binary indicator of transcription Characterization of the genome-wide distribution of H3K36ac using ChIP-seq. Analysis of the mechanistic crosstalk in the deposition of acetylation and methylation at H3K36 by ChIP-seq of H3K36ac and H3K36me3 in sdg8-2 and gcn5-1, respectively.
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Project description:The recognition of modified histones by “reader” proteins constitutes a key mechanism regulating gene expression in the chromatin context. Compared with the great variety of readers for histone methylation, few protein modules that recognize histone acetylation are known. Here we show that the evolutionarily conserved YEATS domains constitute a novel family of acetyllysine readers. The human AF9 YEATS domain binds strongly to histone H3K9 acetylation and, to a lesser extent, H3K27 and H3K18 acetylation. Crystal structural studies revealed that AF9 YEATS adopts an eight-stranded immunoglobin fold and utilizes a serine-lined aromatic “sandwiching” cage for acetyllysine readout, representing a novel recognition mechanism that is distinct from that of known acetyllysine readers. Histone acetylation recognition by AF9 is important for the chromatin recruitment of the H3K79 methyltransferase DOT1L. Together, our studies identify the YEATS domain as a novel acetyllysine-binding module, thereby establishing the first direct link between histone acetylation and DOTL1-mediated H3K79 methylation in transcription control. ChIP-seq analysis of AF9, H3K79me3, H3K9ac in Hela cells and H3K79me3 in Hela AF9 knockdown and Hela Dot1L knockdown cells.
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