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Hda1C restricts burst frequency to limit divergent non-coding transcription

ABSTRACT: Hda1C restricts burst frequency to limit divergent non-coding transcription

PROVIDER: PRJNA704821 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13782634_1.fastq.gz	Fastqsanger.gz
	SRR13782634_2.fastq.gz	Fastqsanger.gz
	SRR13782635_1.fastq.gz	Fastqsanger.gz
	SRR13782635_2.fastq.gz	Fastqsanger.gz
	SRR13782636_1.fastq.gz	Fastqsanger.gz

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Hda1C restricts burst frequency to limit divergent non-coding transcription

Project description:We used Native Elongation Transcript sequencing (NET-seq) to investigate the genome-wide effect of the Hda1 histone deacetylase complex (Hda1C) on the repression of divergent non-coding (DNC) transcription at bidirectional promoters in yeast S.cerevisiae.

2021-08-02 | GSE167499 | GEO

The pause-initiation limit restricts transcription activation in human cells

Project description:Eukaryotic gene transcription is often controlled at the level of RNA polymerase II (Pol II) pausing in the promoter-proximal region. Pausing Pol II limits the frequency of transcription initiation (‘pause-initiation limit’), predicting that the pause duration must be decreased for transcriptional activation. To test this prediction, we conducted a genome-wide kinetic analysis of the heat shock response in human cells. We show that the pause-initiation limit restricts transcriptional activation at most genes. Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency. The transcription of enhancer elements is generally not pause-limited and can be activated without CDK9 activity. Our results define the kinetics of Pol II transcriptional regulation in human cells at all gene classes during a natural transcription response.

2019-07-10 | GSE123980 | GEO

Nutrient Starvation-induced Hda1C Rewiring: coordinated regulation of transcription and translation

Project description:In yeast, Hda1 histone deacetylase complex (Hda1C) plays an important role in transcriptional regulation by modulating histone acetylation. We here explored the dynamics of Hda1C binding in nutrient-rich and -starved conditions. Chromatin immunoprecipitation sequencing revealed that starvation alters RNA Pol II and Hda1C binding to coding genes in a highly correlated manner. Interestingly, we discovered RNA Pol II transcription-independent recruitment of Hda1C to intergenic regions, particularly the upstream regulatory sequences (URS) of ribosomal protein (RP) genes, which are enriched with Rap1 binding sites. Under nutrient starvation, Rap1 contributes to the recruitment of Hda1C to these URS regions, where Hda1C deacetylates histones, thereby fine-tuning basal gene expression and delaying RP gene reactivation. Furthermore, Hda1C is also required for RNA Pol I transcription of rRNAs and RNA Pol III transcription of tRNA genes, especially in nutrient-limited conditions. Significantly, Hda1C mutants are sensitive to translation inhibitors and display altered ribosome profiles. Thus, Hda1C may coordinate transcriptional regulation within the nucleus with translation control in the cytoplasm and could be a key regulator of gene expression responses to nutrient stress.

2025-04-23 | GSE276792 | GEO

The pause-initiation limit restricts transcription activation in human cells

Project description:The pause-initiation limit restricts transcription activation in human cells

| PRJNA510428 | ENA

Transcription-dependent targeting of Hda1C to hyperactive genes mediates H4-specific deacetylation in yeast (RNA-seq)

Project description:Hda1C directly binds to actively transcribed regions likely via the interaction with elongating RNA PolII and/or with nascent RNA transcripts. The Arb2 domain of Hda1 is also critical for its binding to chromatin. Interestingly, Hda1C specifically deacetylates histone H4 but not H3 at active genes to suppress nucleosome instability and partially inhibit elongation. In contrast, Hda1C mainly deacetylates histone H3 at inactive genes to delay gene induction.

2019-07-22 | GSE121762 | GEO

Transcription-dependent targeting of Hda1C to hyperactive genes mediates H4-specific deacetylation in yeast (ChIP-seq)

2019-07-22 | GSE121761 | GEO

PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency

Project description:PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency

| PRJNA668780 | ENA

PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency [ChIP-seq]

Project description:PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency [ChIP-seq]

| PRJNA668782 | ENA

PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency [RNA-seq]

Project description:PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency [RNA-seq]

| PRJNA668783 | ENA

PRC1 drives Polycomb-mediated gene repression by controlling transcription initiation and burst frequency [RNA-seq]

Project description:The Polycomb repressive system plays a fundamental role in controlling gene expression during mammalian development. To achieve this, Polycomb repressive complexes 1 and 2 (PRC1 and PRC2) bind target genes and use histone modification-dependent feedback mechanisms to form Polycomb chromatin domains and repress transcription. The interrelatedness of PRC1 and PRC2 activity at these sites has made it difficult to discover the specific components of Polycomb chromatin domains that drive gene repression and to understand mechanistically how this is achieved. Here, by exploiting rapid degron-based approaches and time-resolved genomics we kinetically dissect Polycomb-mediated repression and discover that PRC1 functions independently of PRC2 to counteract RNA polymerase II binding and transcription initiation. Using single-cell gene expression analysis, we reveal that PRC1 acts uniformly within the cell population, and that repression is achieved by controlling transcriptional burst frequency. These important new discoveries provide a mechanistic and conceptual framework for Polycomb-dependent transcriptional control.

2021-07-21 | GSE159399 | GEO

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