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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identification of transcription factor binding sites from ChIP-seq data at high-resolution

ABSTRACT: Genome-wide mapping of proteinM-bM-^@M-^SDNA interactions is essential for a full understanding of transcriptional regulation. A precise map of binding sites for transcription factors, core transcriptional machinery is vital for deciphering the gene regulatory networks that underlie various biological processes. Chromatin immunoprecipitation followed by sequencing (ChIPM-bM-^@M-^Sseq) is a technique for genome-wide profiling of DNA-binding proteins. However, our conventional ChIPM-bM-^@M-^Sseq occasionally gives wider peaks which might be due to overlapping binding sites of two or more transcription factors. Therefore, to improve the resolution of our conventional ChIPM-bM-^@M-^Sseq which have DNA-protein footprint of ~100 bp, we decreased the size of DNA-protein footprint to ~ 50 bp by DNaseI digestion of whole cell extract (WCE). ChIP-seq for Twist transcription factor in Drosophila embryos

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Samuel Meier

PROVIDER: E-GEOD-40664 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Trans-generationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing [cuff smallRNA]

Project description:Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. small RNA (19-29nt) sequencing of RNA from ovaries of cuff+/- or cuff-/- flies

2014-07-26 | E-GEOD-59608 | biostudies-arrayexpress

Trans-generationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing [cuff RNA-seq]

Project description:Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. total RNA sequencing of RNA from ovaries of cuff+/- or cuff-/- flies

2014-07-26 | E-GEOD-59609 | biostudies-arrayexpress

Tag-seq in eye-antennal and wing imaginal discs of D.melanogaster, D.yakuba, and D.virilis; RNA-seq in wild-type and glass mutant D.melanogaster eye-antennal imaginal discs.

Project description:In this study we use Tag-sequencing in eye-antennal and wing imaginal discs across Drosophila species to determine a set of conserved eye-specific developmental genes. Next, we perform motif discovery analysis using the tool i-cisTarget, to depict the core gene developmental network underlying compound eye photoreceptor. The Glass position weight matrix appears as the most highly overrepresented motif, thus positioning Glass as a master regulator in compound eye photoreceptor development. Differential gene expression analysis by RNA-seq in D.melanogaster wild-type eye-antennal versus glass mutant [gl 60j] shows that the majority of our predicted Glass targets show strong downregulation in the glass mutant. This SuperSeries is composed of the following subset Series: GSE39781: RNA-seq in wild-type and glass mutant eye-antennal discs in Drosophila melanogaster GSE39782: Tag-seq profiling in eye-antennal and wing imaginal discs of D. melanogaster, D. yakuba and D. virilis

2012-09-21 | E-GEOD-39784 | biostudies-arrayexpress

mRNA profile of dG9a-depleted early embryo in Drosophila melanogaster

Project description:Immunocytochemical studies revealed that dG9a moves into nucleus after cycle 8 and appears to regulate gene expression by di-methylating H3K9 from cycle 8 to cycle 11. To determine which genes are regulated by dG9a during cycles 8-11, we examined mRNA levels by performing RNA-sequence analysis using early embryos (0-2 h after egg laying) of dG9a null mutant and wild type as a control mRNA profiles of about 0-2h-old embryos of wild type (CantonS) and dG9a-depleted (dG9aRG5) strain

2015-08-01 | E-GEOD-56665 | biostudies-arrayexpress

Transcriptional and Epigenetic Dynamics During Specification of Human Embryonic Stem Cells

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2013-05-01 | E-GEOD-46130 | biostudies-arrayexpress

Polycomb repressive complex 2-dependent and -independent functions of Jarid2 in transcriptional regulation in Drosophila [ChIP-Seq]

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2012-02-23 | E-GEOD-33546 | 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

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2010-10-20 | E-GEOD-23997 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

Polycomb repressive complex 2-dependent and M-bM-^@M-^Sindependent functions of Jarid2 in transcriptional regulation in Drosophila

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2012-02-23 | E-GEOD-36039 | biostudies-arrayexpress

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