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Mapping binding sites of SIN3 isoforms across the Drosophila genome.

ABSTRACT: SIN3 associates with RPD3 and other accessory proteins to form the SIN3 histone modifying complex. A single Sin3A gene encodes multiple SIN3 isoforms, of which SIN3 187 and SIN3 220 are predominant. Previous studies from our laboratory and others have indicated that SIN3 isoforms play non-redundant roles during fly development, however, the genes regulated by SIN3 isoforms are not known. We mapped the genome-wide binding sites of SIN3 isoforms in Drosophila. We established stable S2 cell lines that express either HA-tagged SIN3 187 or SIN3 220. The binding profiles revealed that the majority of the binding sites of SIN3 isoforms are overlapping. Our data revealed that SIN3 isoforms localize to euchromatic regions of the genome and enrichment of SIN3 isoforms are generally concentrated around the transcription start sites of genes. In addition, the extent of SIN3 binding confirmed previous findings indicating that SIN3 is a global transcriptional regulator. Genome-wide binding analysis of SIN3 187 and SIN3 220 in Drosophila. Using chromatin prepared from cell lines expressing either of the isoforms, we performed chromatin immunoprecipitation on chromatin prepared from cells that expresses either of the isoforms using an antibody against HA (ChIP). We coupled our ChIP with high resolution deep sequencing (ChIP-seq) to identify genomic targets of SIN3 isoforms.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Lori Pile

PROVIDER: E-GEOD-72171 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mapping binding sites of SIN3 isoforms across the Drosophila genome.

Project description:SIN3 associates with RPD3 and other accessory proteins to form the SIN3 histone modifying complex. A single Sin3A gene encodes multiple SIN3 isoforms, of which SIN3 187 and SIN3 220 are predominant. Previous studies from our laboratory and others have indicated that SIN3 isoforms play non-redundant roles during fly development, however, the genes regulated by SIN3 isoforms are not known. We mapped the genome-wide binding sites of SIN3 isoforms in Drosophila. We established stable S2 cell lines that express either HA-tagged SIN3 187 or SIN3 220. The binding profiles revealed that the majority of the binding sites of SIN3 isoforms are overlapping. Our data revealed that SIN3 isoforms localize to euchromatic regions of the genome and enrichment of SIN3 isoforms are generally concentrated around the transcription start sites of genes. In addition, the extent of SIN3 binding confirmed previous findings indicating that SIN3 is a global transcriptional regulator.

2016-01-09 | GSE72171 | GEO

Transcriptome analysis upon overexpression of SIN3 187HA in Drosophila cultured cells

2016-01-09 | GSE72172 | GEO

Transcriptome analysis upon overexpression of SIN3 187HA in Drosophila cultured cells

Project description:SIN3 is a master transcriptional scaffold protein. SIN3 interacts with RPD3 and other accessory proteins to form a histone modifying complex. A single Sin3A gene encodes multiple isoforms of SIN3, of which SIN3 187 and SIN3 220 are the predominant isoforms. Previous studies demonstrated that SIN3 isoforms play non-redundant roles during fly development. In the current study, we sought to investigate the genes regulated by SIN3 187. S2 cells and cells carrying a stable transgene of SIN3 187HA (SIN3 187HA cells) were treated with 0.07 ÂµM CuSO4. CuSO4 treatment led to ectopic expression of SIN3 187HA. S2 cells were used as a control. Following induction, total mRNA was extracted. mRNA profiling of these samples were performed by deep sequencing using Illumina Hiseq2500. Three biological replicates were performed.

2016-01-09 | E-GEOD-72172 | biostudies-arrayexpress

ChIP-seq for ZEB1 in the human breast cancer cell line MDA-MB-231

Project description:Identification of DNA binding sites of the transcription factor ZEB1 in the human breast cancer cell line MDA-MB-231 by chromatin-immunoprecipitation followed by sequencing (ChIP-seq).

2020-07-22 | E-MTAB-8258 | biostudies-arrayexpress

Genome-wide maps of Sin3A and Sin3B binding in C2C12 myoblasts and differentiated myotubes

Project description:Sin3A and Sin3B bind to distinct and overlapping target sites. Sin3 proteins bind to distinct sites in cycling myoblasts whereas there is a converge of Sin3A and Sin3B proteins to sites in differentiated myotubes. We identified a subset of Sin3 target genes involved in muscle differentiation and physiology and showed that conditional ablation of Sin3 proteins in vivo in mouse results in sarcomere defects Examination of Sin3A and Sin3B binding during myogenesis

2011-01-01 | E-GEOD-22554 | biostudies-arrayexpress

Targeting the SIN3A-PF1 Interaction inhibits Epithelial to Mesenchymal Transition and Maintenance of a Stem Cell Phenotype in Triple Negative Breast Cancer (MNase-seq)

Project description:Triple negative breast cancer (TNBC) is characterized by a poorly differentiated phenotype and limited treatment options. Aberrant epigenetics in this subtype represent a potential therapeutic opportunity, but a better understanding of the mechanisms contributing to the TNBC pathogenesis is required. The SIN3 molecular scaffold performs a critical role in multiple cellular processes, including epigenetic regulation, and has been identified as a potential therapeutic target. Using a competitive peptide corresponding to the SIN3 interaction domain of MAD (Tat-SID), we investigated the functional consequences of selectively blocking the paired amphipathic helix (PAH2) domain of SIN3. Here, we report the identification of the SID-containing adaptor PF1 as a factor required for maintenance of the TNBC stem cell phenotype and epithelial to mesenchymal transition (EMT). Tat-SID peptide blocked the interaction between SIN3A and PF1, leading to epigenetic modulation and transcriptional downregulation of TNBC stem cell and EMT markers. Importantly, Tat-SID treatment led to a reduction in primary tumor growth and disseminated metastatic disease in vivo. In support of these findings, knockdown of PF1 expression phenocopied treatment with Tat-SID both in vitro and in vivo. These results demonstrate a critical role for a complex containing SIN3A and PF1 in TNBC and provide a rational for its therapeutic targeting. Mononucleosomes from MDA-MB-231 cells were isolated and ChIP with H3K4me3 antibody. DNA from Input and ChIP samples was purified and sequenced on Illumina Hiseq.

2015-11-02 | E-GEOD-73869 | biostudies-arrayexpress

REF6 recognizes specific DNA sequence to regulate H3K27me3 demethylation and organ boundary formation

Project description:RELATIVE OF EARLY FLOWERING 6 (REF6, also known as JMJ12) counteracts Polycomb mediated gene silencing through demethylating histone H3 lysine 27 trimethylation (H3K27me3) in Arabidopsis. Genome-wide analysis has demonstrated that REF6 dependent H3K37me3 demethylation occurs on hundreds of genes. However, how these genes are selectively subjected to H3K27me3 demethylation remains elusive. Here we show that a tandem array of four Cys2-His2 zinc finger domains (C2H2-ZF) at REF6 C-terminus are essential for REF6 function. Mechanistically, we find that C2H2-ZF cluster can directly recognize a specific DNA sequence motif, and is essential for binding of REF6 to its targets. In addition, we demonstrate that CUP-SHAPED COTYLEDON 1 (CUC1) and CUC3 harbor such sequence motif and are direct targets of REF6; while their close homolog, CUC2, without such binding motif is not bound by REF6. Furthermore, REF6 is essential for proper H3K27me3 level at CUC1 locus, CUC1 activation and cotyledon separation. Collectively, our study reveals not only a novel mechanism of H3K27me3 demethylase genome targeting to counteract Polycomb silencing, but also a new function of H3K27me3 demethylation in organ boundary formation. All seeds, except for H3K9me2 ChIP-seq, were grown on 1/2MS plate at 23Â°C under long day condition. 12 day after germination (12DAG), whole seedling were harvested for ChIP-seq. anti-HA ChIP-seq were performed with three samples: Col (WT,Negtive control), REF6-HA(REF6p::REF6-HA ref6-1),REF6-ZnF-HA(REF6p::REF6-ZnF-HA ref6-1). anti-H3K27me3 ChIP-seq were performed with four samples: Col (WT), ref6-1 (mutant), REF6-HA(REF6p::REF6-HA ref6-1),REF6-ZnF-HA(REF6p::REF6-ZnF-HA ref6-1).For H3K9me2 ChIP-seq, plants were grown in soil at 23Â°C under long day condition. Aerial part of plants were harvested for ChIP-seq 28d after germination.

2016-03-22 | E-GEOD-65329 | biostudies-arrayexpress

Drosophila melanogaster

Project description:Mapping binding sites of SIN3 isoforms across the Drosophila genome.

| PRJNA293235 | ENA

Genome-wide mapping of HIST1H2ac binding sites in MCF-7 cells

Project description:Previously, we have shown that HIST1H2ac is overexpressed in MCF-7 breast cancer cell line. It acts as a master regulator of estrogen receptor alpha-dependent gene expression in ER+ breast cancer cells. In the present study, we investigate the genome-wide protein DNA-binding events of HIST1H2ac protein in MCF-7 breast cancer cell line by over-expressing hemagglutinin (HA)-tagged HIST1H2ac and compared with MCF-7 cells over-expressing HA. The protein-bound DNA was recovered by immunoprecipitation using anti-HA antibody. The ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 sequencer.

2016-05-19 | E-MTAB-3160 | biostudies-arrayexpress

Genome-wide maps of XBP1 binding sites in different breast cancer cell lines [ChIP-Seq]

Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1M-NM-1 motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1M-NM-1, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines. Examination of XBP1 binding sites in 2 cell types (3 cell lines).

2013-09-26 | E-GEOD-49952 | biostudies-arrayexpress

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