Analysis of nascent transcription in ES cells mutant for specific TFIID subunits
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ABSTRACT:
PROVIDER: PRJNA1027343 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26372700.fastq.gz | Fastqsanger.gz | |||
| SRR26372701.fastq.gz | Fastqsanger.gz | |||
| SRR26372702.fastq.gz | Fastqsanger.gz | |||
| SRR26372703.fastq.gz | Fastqsanger.gz | |||
| SRR26372704.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Analysis of nascent transcription in ES cells mutant for specific TFIID subunits [CUT&Run]
| PRJNA1027351 | ENA
Project description:Analysis of nascent transcription in ES cells mutant for specific TFIID subunits [4-sU-Seq]
| PRJNA1027350 | ENA
Project description:RNA polymerase II (Pol II) transcription initiation starts with the assembly of the preinitiation complex (PIC) on core promoters. The PIC is composed of six general transcription factors (GTFs). The recognition of the core promoter sequences by the TFIID GTF complex is the first step of the PIC assembly. In metazoans, holo-TFIID is composed of the TATA binding protein (TBP) and of 13 TBP associated factors (TAFs). Genetic depletion of different murine TAFs have shown that TAFs such as TAF7 or TAF10, can be either required, or dispensable for Pol II transcription, depending on different cellular contexts. In this report, we depleted TAF7 and/or TAF10 in the same cellular system; either in mesodermal progenitors during mouse development or in mESCs. In these two models, TAF7 depletion leads to a milder phenotype compared to TAF10 depletion. As TAF10 is also a subunit of the transcriptional co-activator Spt-Ada-Gcn5 acetyl transferase (SAGA), we first showed that the difference in phenotype between the Taf7 and Taf10 mutant is not due to the SAGA effect, at least for mESCs. Immunoprecipitations coupled with mass spectrometry analyses from mESCs lysates assembly of holo-TFIID complex is rapidly affected after induction of the depletion. In line with the model of holo-TFIID sequential assembly, TAF10 depletion leads to an early defect with formation of the core-TFIID, while TAF7 depletion results in the formation of a TAF7-less TFIID. Thus, the difference in phenotype severity correlates with the degree of TFIID disassembly. Surprisingly, no major global changes in Pol II transcription could be observed after either TAF7 or TAF10 depletion. Our data suggest that the inducible loss of fully assembled canonical TFIID does not correlate with the lack of global Pol II transcription activity changes suggesting that partially assembled TFIID complexes can participate in Pol II transcription initiation, with only limited effect on Pol II nascent transcription.
2024-10-01 | GSE245194 | GEO
Project description:RNA polymerase II (Pol II) transcription initiation starts with the assembly of the preinitiation complex (PIC) on core promoters. The PIC is composed of six general transcription factors (GTFs). The recognition of the core promoter sequences by the TFIID GTF complex is the first step of the PIC assembly. In metazoans, holo-TFIID is composed of the TATA binding protein (TBP) and of 13 TBP associated factors (TAFs). Genetic depletion of different murine TAFs have shown that TAFs such as TAF7 or TAF10, can be either required, or dispensable for Pol II transcription, depending on different cellular contexts. In this report, we depleted TAF7 and/or TAF10 in the same cellular system; either in mesodermal progenitors during mouse development or in mESCs. In these two models, TAF7 depletion leads to a milder phenotype compared to TAF10 depletion. As TAF10 is also a subunit of the transcriptional co-activator Spt-Ada-Gcn5 acetyl transferase (SAGA), we first showed that the difference in phenotype between the Taf7 and Taf10 mutant is not due to the SAGA effect, at least for mESCs. Immunoprecipitations coupled with mass spectrometry analyses from mESCs lysates assembly of holo-TFIID complex is rapidly affected after induction of the depletion. In line with the model of holo-TFIID sequential assembly, TAF10 depletion leads to an early defect with formation of the core-TFIID, while TAF7 depletion results in the formation of a TAF7-less TFIID. Thus, the difference in phenotype severity correlates with the degree of TFIID disassembly. Surprisingly, no major global changes in Pol II transcription could be observed after either TAF7 or TAF10 depletion. Our data suggest that the inducible loss of fully assembled canonical TFIID does not correlate with the lack of global Pol II transcription activity changes suggesting that partially assembled TFIID complexes can participate in Pol II transcription initiation, with only limited effect on Pol II nascent transcription.
2024-10-01 | GSE245195 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-10-01 | GSE245196 | GEO
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Three iPS lines, iPS#1, iPS#4, and iPS#5 were used in duplicate for microarray analysis against a pool of RNA from ES-cells.
2013-03-21 | E-GEOD-33645 | biostudies-arrayexpress
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Two Taf5 knockdown cell lines and two control knockdown lines were each grown in duplicate and analysed on microarray against a pool of RNA from the parental ES-cells
2013-03-21 | E-GEOD-33644 | biostudies-arrayexpress
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states.
2013-03-21 | GSE33645 | GEO
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states.
2013-03-21 | GSE33644 | GEO
Project description:TFIID is a cornerstone of eukaryotic gene regulation. Distinct TFIID complexes with unique subunit composition exist and several TFIID subunits are shared with other complexes, conveying intricate cellular decision making to control subunit allocation and functional assembly of this essential transcription factor. However, the underlying molecular mechanisms remain poorly understood. Here, we used quantitative proteomics to examine TFIID submodules and assembly mechanisms in human cells. Structural and mutational analysis of the cytoplasmic TAF5/TAF6/TAF9 submodule identified novel interactions crucial for TFIID integrity, and for allocating TAF9 to TFIID or the SAGA co-activator complex. We discover a key checkpoint function for the chaperonin CCT, which specifically associates with nascent TAF5 for subsequent handover to TAF6/TAF9 and ultimate holo-TFIID formation. Our findings illustrate at the molecular level how multisubunit complexes are crafted in the cell, involving checkpoint decisions facilitated by a chaperone machine.
2022-03-02 | PXD011211 | Pride