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

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

PROVIDER: PRJNA854939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19924946_1.fastq.gz	Fastqsanger.gz
	SRR19924946_2.fastq.gz	Fastqsanger.gz
	SRR19924947_1.fastq.gz	Fastqsanger.gz
	SRR19924947_2.fastq.gz	Fastqsanger.gz
	SRR19924948_1.fastq.gz	Fastqsanger.gz

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Two separate roles for the transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA [ChEC-Seq]

Project description:Deletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.

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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.

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Two separate roles for the transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA [RNA]

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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.

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

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

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Two separate roles for the transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA [ChEC-Seq]

Project description:Two separate roles for the transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA [ChEC-Seq]

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The SAGA coactivator regulates the expression of nearly all genes transcribed by RNA polymerase II

Project description:The SAGA coactivator complex facilitates transcription initiation through chromatin-modifying activities and interaction with TBP. SAGA was suggested to regulate the expression of about 10% of yeast genes, leading to the longstanding distinction of SAGA-dominated from TFIID-dominated genes, depending on the complex used to recruit TBP to promoters. We reassessed the genome-wide localization of SAGA by using ChEC-seq and its role on transcription through quantification of newly-synthesized mRNA. Here we show that SAGA binds to the upstream activating sequences of a majority of yeast genes. Deletion analyses reveal a global role for SAGA in transcription and a synergistic effect of Spt3 (TBP-binding subunit) with the acetyltransferase Gcn5. Our data demonstrate that SAGA acts as a general cofactor required for essentially all RNA polymerase II transcription. Hence, differential gene regulation, largely attributed to either SAGA or TFIID dominancy, is not accurate, but instead depends on other features of genes promoters.

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