Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274712 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1791520_1.fastq.gz | Fastqsanger.gz | |||
| SRR1791520_2.fastq.gz | Fastqsanger.gz | |||
| SRR1791521_1.fastq.gz | Fastqsanger.gz | |||
| SRR1791521_2.fastq.gz | Fastqsanger.gz | |||
| SRR1791522_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Tat controls RNA Polymerase II and the epigenetic landscape to precisely rewire cellular transcriptional programs
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Project description:Tat controls RNA Polymerase II and the epigenetic landscape to precisely rewire cellular transcriptional programs (ChIP-Seq)
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Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation. Tat vs. GFP
2015-06-15 | E-GEOD-65688 | biostudies-arrayexpress
Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation. ChIP of various DNA binding proteins
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Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation.
2015-06-15 | GSE65687 | GEO
Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation.
2015-06-15 | GSE65688 | GEO
Project description:<p>Non-coding elements in our genomes that play critical roles in complex disease are frequently marked by highly unstable RNA species. Sequencing nascent RNAs attached to an actively transcribing RNA polymerase complex can identify unstable RNAs, including those templated from gene-distal enhancers (eRNAs). However, nascent RNA sequencing techniques remain challenging to apply in some cell lines and especially to intact tissues, limiting broad applications in fields such as cancer genomics and personalized medicine. Here we report the development of chromatin run-on and sequencing (ChRO-seq), a novel run-on technology that maps the location of RNA polymerase using virtually any frozen tissue sample, including samples with degraded RNA that are intractable to conventional RNA-seq. We used ChRO-seq to develop the first maps of nascent transcription in 23 human glioblastoma (GBM) brain tumors and patient derived xenografts. Remarkably, >90,000 distal enhancers discovered using the signature of eRNA biogenesis within primary GBMs closely resemble those found in the normal human brain, and diverge substantially from GBM cell models. Despite extensive overall similarity, 12% of enhancers in each GBM distinguish normal and malignant brain tissue. These enhancers drive regulatory programs similar to the developing nervous system and are enriched for transcription factor binding sites that specify a stem-like cell fate. These results demonstrate that GBMs largely retain the enhancer landscape associated with their tissue of origin, but selectively adopt regulatory programs that are responsible for driving stem-like cell properties. We also identified enhancers and their associated transcription factors that regulate genes characteristic of each known GBM subtype, and discovered a core group of transcription factors that control the expression of genes associated with clinical outcomes. This study uncovers new insights into the molecular etiology of GBM and introduces ChRO-seq which can now be used to map regulatory programs contributing to a variety of complex diseases.</p>
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