Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Enhancer chromatin signatures predict Smad2/3 binding in Xenopus

ABSTRACT: In this study we have examine the deposition of H3K4me1,H3K4Me3 and H3K27Ac and the Nodal transcription factor, Smad2/3, immediately following zygotic transcription and continuing through gastrulation. We profiled 4 histone modifications (H3K4Me3, H3K27Me3, H3K27AC, H3K4Me1) and one transcription factor smad2/3 (+ chromatin input) using ChIP-Seq, and expression profiles (3' RNA-Seq) for Xenopus tropicalis embryos stage8, stage9 and stage10.5. Furthermore, we have profile two histone modifications (H3K4Me1 and H3K27Ac) in absance of nodal signaling in stage9 Xenopus tropicalis embryos using ChIP-seq and 3-seq

ORGANISM(S): Xenopus (Silurana) tropicalis

SUBMITTER: Julie Baker

PROVIDER: E-GEOD-56000 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Developmental enhancers are marked independently of zygotic Nodal signals in Xenopus.

Gupta Rakhi R Wills Andrea A Ucar Duygu D Baker Julie J

Developmental biology 20140906 1

To determine the hierarchy of transcriptional regulation within the in vivo vertebrate embryo, we examined whether developmental enhancers were influenced by Nodal signaling during early embryogenesis in Xenopus tropicalis. We find that developmental enhancers, defined by the active enhancer chromatin marks H3K4me1 and H3K27ac, are established as early as blastula stage and that Smad2/3 only strongly associates with these regions at gastrula stages. Significantly, when we perturb Nodal signaling ...[more]

PMID: 25205067

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Project description:Genome-wide association studies (GWAS) have revolutionized the field of cancer genetics, but the causal links between increased genetic risk and onset/progression of disease processes remain to be identified. Here we report the first step in such an endeavor for prostate cancer. We provide a comprehensive annotation of the 77 known risk loci, based upon highly correlated variants in biologically relevant chromatin annotations- we identified 727 such potentially functional SNPs. We also provide a detailed account of possible protein disruption, microRNA target sequence disruption and regulatory response element disruption of all correlated SNPs at r^2≥0.5. Greater than 88% of the 727 SNPs fall within putative enhancers, many of which alter critical residues in the response elements of transcription factors known to be involved in prostate biology. We define as risk enhancers those regions with enhancer chromatin biofeatures in prostate-derived cell lines with prostate-cancer correlated SNPs. To aid in the identification of these enhancers, we performed genomewide ChIP-seq for H3K27-acetylation, a mark of actively engaged enhancer regions, as well as the transcription factor TCF7L2. We analyzed in depth three variants in risk enhancers, two of which show significantly altered androgen sensitivity in LNCaP cells. This includes rs4907792, that is in linkage disequilibrium (r^2=0.91) with an eQTL for NUDT11 (on the X chromosome) in prostate tissue, and rs10486567, the index SNP in intron 3 of the JAZF1 gene on chromosome 7. Rs4907792 is within a critical residue of a strong consensus androgen response element that is interrupted in the protective allele, resulting in a 56% decrease in its androgen sensitivity, whereas rs10486567 affects both NKX3-1 and FOXA-AR motifs where the risk allele results in a 39% increase in basal activity and a 28% fold-increase in androgen stimulated enhancer activity. Identification of such enhancer variants and their potential target genes represents a preliminary step in connecting risk to disease process. ChIP-seq analysis of H3K27Ac in LNCaP charcoal-stripped serum, H3K27Ac in LNCaP charcoal-stripped serum +DHT, TCF7L2 in LNCaP

Dataset Information

Enhancer chromatin signatures predict Smad2/3 binding in Xenopus

Publications

Developmental enhancers are marked independently of zygotic Nodal signals in Xenopus.

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