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Binding site turnover produces pervasive quantitative changes in TF binding between closely related Drosophila species

ABSTRACT: Binding site turnover produces pervasive quantitative changes in TF binding between closely related Drosophila species

PROVIDER: PRJNA125469 | ENA |

REPOSITORIES: ENA

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Binding site turnover produces pervasive quantitative changes in TF binding between closely related Drosophila species

Project description:[original title] Binding site turnover produces pervasive quantitative changes in transcription factor binding between closely related Drosophila species. We demonstrate extensive quantitative changes in binding of six factors that control early embryonic patterning between two closely related Drosophila species ChIP-Seq based binding measurements of six transcription factors in embryos of two Drosophila species, D.melanogaster and D.yakuba.

2010-02-18 | E-GEOD-20369 | biostudies-arrayexpress

Binding site turnover produces pervasive quantitative changes in TF binding between closely related Drosophila species

2010-02-18 | GSE20369 | GEO

Binding site turnover produces pervasive quantitative changes in transcription factor binding between closely related Drosophila species.

Project description:Changes in gene expression play an important role in evolution, yet the molecular mechanisms underlying regulatory evolution are poorly understood. Here we compare genome-wide binding of the six transcription factors that initiate segmentation along the anterior-posterior axis in embryos of two closely related species: Drosophila melanogaster and Drosophila yakuba. Where we observe binding by a factor in one species, we almost always observe binding by that factor to the orthologous sequence in the other species. Levels of binding, however, vary considerably. The magnitude and direction of the interspecies differences in binding levels of all six factors are strongly correlated, suggesting a role for chromatin or other factor-independent forces in mediating the divergence of transcription factor binding. Nonetheless, factor-specific quantitative variation in binding is common, and we show that it is driven to a large extent by the gain and loss of cognate recognition sequences for the given factor. We find only a weak correlation between binding variation and regulatory function. These data provide the first genome-wide picture of how modest levels of sequence divergence between highly morphologically similar species affect a system of coordinately acting transcription factors during animal development, and highlight the dominant role of quantitative variation in transcription factor binding over short evolutionary distances.

| S-EPMC2843597 | biostudies-literature

Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization

Project description:Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization

| PRJNA1018867 | ENA

Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription

Project description:Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-based Regulation of Transcription

| PRJNA491670 | ENA

Pervasive TTP binding but selective target mRNA destabilization in the macrophage transcriptome [PAR-iCLIP]

Project description:Precise control of mRNA decay is fundamental for robust yet not exaggerated inflammatory responses to pathogens. Parameters determining the specificity and extent of mRNA degradation within the entire inflammation-associated transcriptome remain incompletely understood. Using transcriptome-wide high resolution occupancy assessment of the mRNA-destabilizing protein TTP, a major inflammation-limiting factor, we qualitatively and quantitatively characterize TTP binding positions and functionally relate them to TTP-dependent mRNA decay in immunostimulated macrophages. We identify pervasive TTP binding with incompletely penetrant linkage to mRNA destabilization. A necessary but not sufficient feature of TTP-mediated mRNA destabilization is binding to 3â untranslated regions (UTRs). Mapping of binding positions of the mRNA-stabilizing protein HuR in activated macrophages revealed that TTP and HuR binding sites in 3â UTRs occur mostly in different transcripts implicating only a limited co-regulation of inflammatory mRNAs by these proteins. Remarkably, we identify robust and widespread TTP binding to introns of stable transcripts. Nuclear TTP is associated with spliced-out introns and maintained in the nucleus throughout the inflammatory response. Our study establishes a functional annotation of binding positions dictating TTP-dependent mRNA decay in immunostimulated macrophages. The findings allow navigating the transcriptome-wide landscape of RNA elements controlling inflammation. PAR-iCLIP for TTP (3 replicates) and for HuR (2 replicates)

2016-05-17 | E-GEOD-63466 | biostudies-arrayexpress

Pervasive TTP binding but selective target mRNA destabilization in the macrophage transcriptome [RNA-Seq]

Project description:Precise control of mRNA decay is fundamental for robust yet not exaggerated inflammatory responses to pathogens. Parameters determining the specificity and extent of mRNA degradation within the entire inflammation-associated transcriptome remain incompletely understood. Using transcriptome-wide high resolution occupancy assessment of the mRNA-destabilizing protein TTP, a major inflammation-limiting factor, we qualitatively and quantitatively characterize TTP binding positions and functionally relate them to TTP-dependent mRNA decay in immunostimulated macrophages. We identify pervasive TTP binding with incompletely penetrant linkage to mRNA destabilization. A necessary but not sufficient feature of TTP-mediated mRNA destabilization is binding to 3â untranslated regions (UTRs). Mapping of binding positions of the mRNA-stabilizing protein HuR in activated macrophages revealed that TTP and HuR binding sites in 3â UTRs occur mostly in different transcripts implicating only a limited co-regulation of inflammatory mRNAs by these proteins. Remarkably, we identify robust and widespread TTP binding to introns of stable transcripts. Nuclear TTP is associated with spliced-out introns and maintained in the nucleus throughout the inflammatory response. Our study establishes a functional annotation of binding positions dictating TTP-dependent mRNA decay in immunostimulated macrophages. The findings allow navigating the transcriptome-wide landscape of RNA elements controlling inflammation. RNA-Seq of RNA isolated from murine bone marrow derived macrophages (WT or TTP-deficient) stimulated for 6 h with LPS

2016-05-17 | E-GEOD-63467 | biostudies-arrayexpress

Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization [Hi-C]

Project description:Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization [Hi-C]

| PRJNA1018870 | ENA

Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization [ChIP-seq]

Project description:Pervasive RNA Binding Protein Enrichment on TAD Boundaries Regulates TAD Organization [ChIP-seq]

| PRJNA1018473 | ENA

Pervasive TTP binding but selective target mRNA destabilization in the macrophage transcriptome [RNA-Seq_2]

Project description:Precise control of mRNA decay is fundamental for robust yet not exaggerated inflammatory responses to pathogens. Parameters determining the specificity and extent of mRNA degradation within the entire inflammation-associated transcriptome remain incompletely understood. Using transcriptome-wide high resolution occupancy assessment of the mRNA-destabilizing protein TTP, a major inflammation-limiting factor, we qualitatively and quantitatively characterize TTP binding positions and functionally relate them to TTP-dependent mRNA decay in immunostimulated macrophages. We identify pervasive TTP binding with incompletely penetrant linkage to mRNA destabilization. A necessary but not sufficient feature of TTP-mediated mRNA destabilization is binding to 3â?? untranslated regions (UTRs). Mapping of binding positions of the mRNA-stabilizing protein HuR in activated macrophages revealed that TTP and HuR binding sites in 3â?? UTRs occur mostly in different transcripts implicating only a limited co-regulation of inflammatory mRNAs by these proteins. Remarkably, we identify robust and widespread TTP binding to introns of stable transcripts. Nuclear TTP is associated with spliced-out introns and maintained in the nucleus throughout the inflammatory response. Our study establishes a functional annotation of binding positions dictating TTP-dependent mRNA decay in immunostimulated macrophages. The findings allow navigating the transcriptome-wide landscape of RNA elements controlling inflammation. Experiment comparing RNA decay rates in WT and TTP-/- macrophages at LPS 3 h and 6 h. Transcription was blocked with actinomycin D for 0, 45 or 90 min. Decay rates was calculated using linear model.

2016-05-17 | E-GEOD-78209 | biostudies-arrayexpress

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