Ontology highlight
ABSTRACT:
PROVIDER: PRJNA256322 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1528600.fastq.gz | Fastqsanger.gz | |||
| SRR1528601.fastq.gz | Fastqsanger.gz | |||
| SRR1528602.fastq.gz | Fastqsanger.gz | |||
| SRR1528603.fastq.gz | Fastqsanger.gz | |||
| SRR1528594.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:Transcriptional Pause Release Is a Rate-Limiting Step for Somatic Cell Reprogramming (RNA-seq)
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Project description:Transcriptional Pause Release Is a Rate-Limiting Step for Somatic Cell Reprogramming (ChIP-seq)
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Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release. Pol II ChIP-seq for MEFs, ESCs and bulk populations of OSKM reprogramming intermediates at two time points.
2014-10-07 | E-GEOD-59828 | biostudies-arrayexpress
Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release. Examination of differential gene expression after overexpression of Cdk9-DN at 4 time points of somatic cell reprogramming
2014-10-07 | E-GEOD-59813 | biostudies-arrayexpress
Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release. Refer to individual Series
2014-10-07 | E-GEOD-59833 | biostudies-arrayexpress
Project description:RNA Polymerase II (RNAPII) pausing immediately downstream of the transcription start site (TSS) is a critical rate limiting step for the induction of most metazoan genes. During pause-release, RNAPII encounters a highly conserved +1 H2A.Z nucleosome, yet how this histone variant contributes to transcription is poorly understood. Here, using an inducible protein degron system combined with genomic approaches and live cell super-resolution microscopy, we show that H2A.Z.1 modulates RNAPII dynamics across most genes in murine embryonic stem cells (ESCs). Our quantitative analysis shows that H2A.Z.1 slows the rate of RNAPII pause release and consequently impacts Negative Elongation Factor (NELF) dynamics as well as nascent transcription. Consequently, H2A.Z.1 also impacts re-loading of the Pre-Initiation Complex (PIC) components TFIIB and TBP. Together, this work provides a critical mechanistic link between H2A.Z.1 and the proper induction of mammalian gene expression programs by regulating RNAPII dynamics and pause release.
2021-04-03 | GSE143737 | GEO
Project description:RNA polymerase II promoter-proximal pausing is orchestrated by a ribonucleoprotein complex scaffolded by the noncoding RNA Rn7sk. However, how this interruption of transcription is mechanistically linked to RNA production remains largely unknown. Here, we show that forcing the pause release by germ-line deletion of Rn7sk was embryonic lethal, yet conditional deletion of Rn7sk enhanced stem cell differentiation in skin. To explore the immediate transcriptional mechanisms underpinning enhanced differentiation, we metabolically labelled newly-synthesized RNAs after Rn7sk deletion. Unexpectedly, forced pause release robustly repressed transcription specifically at cell cycle regulators, in the absence of chromatin remodeling at promoters and enhancers. Our results indicate that polymerase pausing affords the core elongation machinery time to properly assemble, and forced elongation triggers splicing defects and nuclear RNA decay. Cell cycle regulators appear highly sensitive to mis-regulation of the elongation machinery due to unique genomic features of high promoter accessibility and low GC–content in the gene body. Transcriptional pausing thus serves as a rate-limiting step in controlling cell division.
2021-08-12 | GSE101215 | GEO
Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release.
2014-10-07 | GSE59828 | GEO
Project description:RNA polymerase II promoter-proximal pausing is orchestrated by a ribonucleoprotein complex scaffolded by the noncoding RNA Rn7sk. However, how this interruption of transcription is mechanistically linked to RNA production remains largely unknown. Here, we show that forcing the pause release by germ-line deletion of Rn7sk was embryonic lethal, yet conditional deletion of Rn7sk enhanced stem cell differentiation in skin. To explore the immediate transcriptional mechanisms underpinning enhanced differentiation, we metabolically labelled newly-synthesized RNAs after Rn7sk deletion. Unexpectedly, forced pause release robustly repressed transcription specifically at cell cycle regulators, in the absence of chromatin remodeling at promoters and enhancers. Our results indicate that polymerase pausing affords the core elongation machinery time to properly assemble, and forced elongation triggers splicing defects and nuclear RNA decay. Cell cycle regulators appear highly sensitive to mis-regulation of the elongation machinery due to unique genomic features of high promoter accessibility and low GC–content in the gene body. Transcriptional pausing thus serves as a rate-limiting step in controlling cell division.
2021-08-12 | GSE101216 | GEO
Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release.
2014-10-07 | GSE59813 | GEO