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H2A.Z marks the 5' end of genes

ABSTRACT: In S. cerevisiae, histone variant H2A.Z is deposited in euchromatin at the flanks of silent heterochromatin to prevent its ectopic spread. The degree to which H2A.Z is found and functions elsewhere is unknown. Here we show that H2A.Z nucleosomes are found at promoter regions of nearly all genes in euchromatin. They generally occur as two positioned nucleosomes that flank a nucleosome-free region (NFR) that contains the transcription start site. Astonishingly, enrichment at 5’ ends is independent of transcriptional state as it is observed not only at actively transcribed genes, but also at inactive loci. Mutagenesis of a typical promoter revealed a 22 bp segment of DNA sufficient to program formation of a NFR flanked by two H2A.Z nucleosomes. This segment contains a binding site of the Myb-related protein Reb1 and an adjacent dT:dA tract. Efficient deposition of H2A.Z is further promoted by a specific pattern of histone H3 and H4 tail acetylation and the bromodomain protein Bdf1, a component of the Swr1 complex that deposits H2A.Z. These data define DNA- and histone-based mechanisms by which dividing cells define the 5’ ends of genes and preserve their euchromatic state in the absence of transcription. Keywords: ChIP-chip

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE3411 | GEO | 2005/10/07

SECONDARY ACCESSION(S): PRJNA93433

REPOSITORIES: GEO

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Chromatin immunoprecipitation of wild type msc1D and swr1D fission yeast to determine genome-wide distribution of H2A.Z

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H2A.Z marks antisense promoters and has positive effects on antisense transcript levels in budding yeast

Project description:The histone variant H2A.Z, which has been reported to have both activating and repressive effects on gene expression, is known to occupy nucleosomes at the 5’ ends of protein-coding genes. We now find that H2A.Z is also significantly enriched in gene coding regions and at the 3’ ends of genes in budding yeast, where it co-localises with histone marks associated with active promoters. By comparing H2A.Z binding to global gene expression in budding yeast strains engineered so that normally unstable transcripts are abundant, we show that H2A.Z is required for normal levels of antisense transcripts as well as sense ones. High levels of H2A.Z at antisense promoters are associated with decreased antisense transcript levels when H2A.Z is deleted, indicating that H2A.Z has an activating effect on antisense transcripts. Decreases in antisense transcripts affected by H2A.Z are accompanied by increased levels of paired sense transcripts. Therefore, the effect of H2A.Z on protein coding gene expression is a reflection of its importance for normal levels of both sense and antisense transcripts. Htz1 ChIP-seq in wild-type (WT) and rrp6Δ yeast, along with negative control ChIP-seq in htz1Δ and input control. Strand-specific transcriptomic profiles of WT, htz1Δ, rrp6Δ and htz1Δrrp6Δ. Replicates are present for all samples except the negative and input control ChIP samples.

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Chromatin dynamics and the RNA exosome function in concert to regulate transcriptional homeostasis (ChIP-seq)

Project description:The histone variant H2A.Z is a hallmark of nucleosomes flanking the promoters of protein coding genes, and is often found in nucleosomes that also carry lysine 56- acetylated histone H3 (H3-K56Ac), a mark which promotes rapid replication- independent turnover of nucleosomes. Although H2A.Z and H3-K56Ac have been generally implicated in transcriptional activation, their exact contributions have remained elusive. Here we find that H3-K56Ac promotes RNA polymerase II occupancy at a large number of protein coding and noncoding loci, yet neither H3- K56Ac nor H2A.Z has a significant impact on steady state mRNA levels in yeast. Instead, broad effects of H3-K56Ac or H2A.Z on levels of both coding and noncoding RNAs (ncRNAs) are only revealed in the absence of the nuclear RNA exosome. H2A.Z is also necessary for expression of divergent, promoter-proximal ncRNAs in mouse embryonic stem cells, suggesting a conserved role for H2A.Z across eukaryotes. Finally, we show that H2A.Z functions with H3-K56Ac in chromosome folding, facilitating formation of chromosome interaction domains (CIDs). Our study suggests that H2A.Z and H3-K56Ac work in concert with the RNA exosome to control mRNA and ncRNA expression, perhaps in part by regulating higher order chromatin structures. 2 replicates of WT (CY1089), rtt109â (CY2210), rrp6â (CY2071) and one replicate of the W303 input (Sample 7). TableS5.xlsx contains the processed IP/input values for each ORF transcript.

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H2A.Z marks antisense promoters and has positive effects on antisense transcript levels in budding yeast

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