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Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters

ABSTRACT: Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters

PROVIDER: PRJNA717787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14083700_1.fastq.gz	Fastqsanger.gz
	SRR14083700_2.fastq.gz	Fastqsanger.gz
	SRR14083701_1.fastq.gz	Fastqsanger.gz
	SRR14083701_2.fastq.gz	Fastqsanger.gz
	SRR14083702_1.fastq.gz	Fastqsanger.gz

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Connection of core and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChIP-Seq]

Project description:Connection of core and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChIP-Seq]

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Connection of core and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChIP-Seq]

Project description:The Mediator coactivator complex is divided into four modules: head, middle, tail, and kinase. Deletion of the architectural subunit Med16 separates core Mediator (cMed), comprising the head, middle, and scaffold (Med14), from the tail. However, the direct global effects of tail/cMed disconnection are unclear. We find that rapid depletion of Med16 downregulates genes that require the SAGA complex for full expression, consistent with their reported tail dependence, but also moderately overactivates TFIID-dependent genes in a manner partly dependent on the separated tail, which remains associated with upstream activating sequences. Suppression of TBP dynamics via removal of the Mot1 ATPase partially restores normal transcriptional activity to Med16-depleted cells, suggesting that cMed/tail separation results in an imbalance in the levels of PIC formation at SAGA-requiring and TFIID-dependent genes. We suggest that the preferential regulation of SAGA-requiring genes by tailed Mediator helps maintain a proper balance of transcription between these genes and those more dependent on TFIID.

2021-07-30 | GSE171981 | GEO

Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [nsRNA-seq]

Project description:Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [nsRNA-seq]

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Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq]

Project description:Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq]

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Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [nsRNA-seq]

Project description:The Mediator coactivator complex is divided into four modules: head, middle, tail, and kinase. Deletion of the architectural subunit Med16 separates core Mediator (cMed), comprising the head, middle, and scaffold (Med14), from the tail. However, the direct global effects of tail/cMed disconnection are unclear. We find that rapid depletion of Med16 downregulates genes that require the SAGA complex for full expression, consistent with their reported tail dependence, but also moderately overactivates TFIID-dependent genes in a manner partly dependent on the separated tail, which remains associated with upstream activating sequences. Suppression of TBP dynamics via removal of the Mot1 ATPase partially restores normal transcriptional activity to Med16-depleted cells, suggesting that cMed/tail separation results in an imbalance in the levels PIC formation at SAGA-requiring and TFIID-dependent genes. We suggest that the preferential regulation of SAGA-requiring genes by tailed Mediator helps maintain a proper balance of transcription between these genes and those more dependent on TFIID.

2021-07-30 | GSE169747 | GEO

Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq]

Project description:The Mediator coactivator complex is divided into four modules: head, middle, tail, and kinase. Deletion of the architectural subunit Med16 separates core Mediator (cMed), comprising the head, middle, and scaffold (Med14), from the tail. However, the direct global effects of tail/cMed disconnection are unclear. We find that rapid depletion of Med16 downregulates genes that require the SAGA complex for full expression, consistent with their reported tail dependence, but also moderately overactivates TFIID-dependent genes in a manner partly dependent on the separated tail, which remains associated with upstream activating sequences. Suppression of TBP dynamics via removal of the Mot1 ATPase partially restores normal transcriptional activity to Med16-depleted cells, suggesting that cMed/tail separation results in an imbalance in the levels PIC formation at SAGA-requiring and TFIID-dependent genes. We suggest that the preferential regulation of SAGA-requiring genes by tailed Mediator helps maintain a proper balance of transcription between these genes and those more dependent on TFIID.

2021-07-30 | GSE169746 | GEO

Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq Med16-AID]

Project description:The Mediator coactivator complex is divided into four modules: head, middle, tail, and kinase. Deletion of the architectural subunit Med16 separates core Mediator (cMed), comprising the head, middle, and scaffold (Med14), from the tail. However, the direct global effects of tail/cMed disconnection are unclear. We find that rapid depletion of Med16 downregulates genes that require the SAGA complex for full expression, consistent with their reported tail dependence, but also moderately overactivates TFIID-dependent genes in a manner partly dependent on the separated tail, which remains associated with upstream activating sequences. Suppression of TBP dynamics via removal of the Mot1 ATPase partially restores normal transcriptional activity to Med16-depleted cells, suggesting that cMed/tail separation results in an imbalance in the levels PIC formation at SAGA-requiring and TFIID-dependent genes. We suggest that the preferential regulation of SAGA-requiring genes by tailed Mediator helps maintain a proper balance of transcription between these genes and those more dependent on TFIID.

2021-07-30 | GSE179765 | GEO

Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq Med16-AID]

Project description:Connection of core and and tail Mediator modules restrains transcription from TFIID-dependent promoters [ChEC-seq Med16-AID]

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Connection of core and tail Mediator modules restrains transcription from TFIID-dependent promoters.

Project description:The Mediator coactivator complex is divided into four modules: head, middle, tail, and kinase. Deletion of the architectural subunit Med16 separates core Mediator (cMed), comprising the head, middle, and scaffold (Med14), from the tail. However, the direct global effects of tail/cMed disconnection are unclear. We find that rapid depletion of Med16 downregulates genes that require the SAGA complex for full expression, consistent with their reported tail dependence, but also moderately overactivates TFIID-dependent genes in a manner partly dependent on the separated tail, which remains associated with upstream activating sequences. Suppression of TBP dynamics via removal of the Mot1 ATPase partially restores normal transcriptional activity to Med16-depleted cells, suggesting that cMed/tail separation results in an imbalance in the levels of PIC formation at SAGA-requiring and TFIID-dependent genes. We propose that the preferential regulation of SAGA-requiring genes by tailed Mediator helps maintain a proper balance of transcription between these genes and those more dependent on TFIID.

| S-EPMC8384189 | biostudies-literature

Involvement of the SAGA and TFIID coactivator complexes in transcriptional dysregulation caused by separation of core and tail Mediator modules (ChEC-Seq)

Project description:Regulation of RNA polymerase II (RNAPII) transcription requires the concerted efforts of several multisubunit coactivator complexes, which interact with the RNAPII preinitiation complex (PIC) to stimulate transcription. We previously showed that separation of the Mediator core (cMed) from Mediator’s tail module results in modest overactivation of genes annotated as highly dependent on TFIID for expression. However, it is unclear if other coactivators are involved in this phenomenon. Here, we show that the overactivation of certain genes by cMed/tail separation is blunted by disruption of the SAGA complex through removal of its structural Spt20 subunit, though this downregulation does not appear to depend on reduced SAGA association with the genome. Consistent with the enrichment of TFIID-dependent genes among genes overactivated by cMed/tail separation, depletion of the essential TFIID subunit Taf13 suppressed overactivation of these genes when Med16 was simultaneously removed. As with SAGA, this effect did not appear to be dependent on reduced genomic association of TFIID. Given that the observed changes in gene expression could not be clearly linked to alterations in SAGA or TFIID occupancy, our data may suggest that the cMed/tail connection is important for modulation of SAGA and/or TFIID conformation and/or function at target genes.

2022-10-03 | GSE207369 | GEO

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