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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.

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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.

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The pause-initiation limit restricts transcription activation in human cells

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

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

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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]

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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.

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

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WRKY6 Transcription Factor Restricts Arsenate Uptake and Transposon Activation in Arabidopsis

Project description:Stress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing. Three biological replicates were performed for each sample type. Single channel hybridizations were carried-out using either Affymetrix ATH1 platform or Nimblegen Gene Expression 12x135K platform (Arabidopsis thaliana).

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