RNA Polymerase II coordinates histone deacetylation at active promoters
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1160989 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30665200_1.fastq.gz | Fastqsanger.gz | |||
| SRR30665200_2.fastq.gz | Fastqsanger.gz | |||
| SRR30665300_1.fastq.gz | Fastqsanger.gz | |||
| SRR30665300_2.fastq.gz | Fastqsanger.gz | |||
| SRR30665201_1.fastq.gz | Fastqsanger.gz |
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Project description:Nucleosomes at actively transcribed promoters have specific histone post-transcriptional modifications and histone variants. These features are thought to contribute to the formation and maintenance of a permissive chromatin environment. Recent reports have drawn conflicting conclusions about whether these histone modifications depend on transcription. We used triptolide to inhibit transcription initiation and degrade RNA Polymerase II and interrogated the effect on histone modifications. Transcription initiation was dispensable for de novo and steady-state histone acetylation at transcription start sites (TSSs) and enhancers. However, at steady state, blocking transcription initiation increased the levels of histone acetylation and H2AZ incorporation at active TSSs. These results demonstrate that deposition of specific histone modifications at TSSs is not dependent on transcription and that transcription limits the maintenance of these marks.
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Project description:Our ability to understand the control logic embedded in the human genome is limited by a lack of accurate information of the promoter sequences for most genes. Promoters are a unique class of control sequences, serving as the binding sites for both sequence-specific factors and the general transcription machinery during transcription initiation. In order to obtain a comprehensive map of promoters in the human genome, we have determined the location of the RNA polymerase II preinitiation complex throughout the non-repeat sequences of the human genome in primary fibroblast cells. The resulting map defines 10,571 active promoters corresponding to 6,763 known genes and at least 1,199 un-annotated transcriptional units. The map indicates extensive usage of multiple promoters by the human genes and widespread clustering of active promoters in the genome. Further examination of the genome-wide expression profile reveals four general classes of promoters that define the transcriptome of the cell. Our results provide a global view of the functional relationship among the transcriptional machinery, chromatin structure, and gene expression in human cells. Keywords = GALA Keywords = gene expression Keywords = nimblegen Keywords = promoter profile Keywords = LICR renlab Keywords: other
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Project description:MYC family proteins are oncogenic transcription factors that can globally affect the function of RNA Polymerase II (RNAPII). The ability of MYC proteins to promote transcription elongation depends on their ubiquitination, but the underlying mechanism and its biological relevance are unknown. Here we show that MYC and the Polymerase II associated factor, PAF1c, interact directly and their function is mutually dependent, since the specific binding of MYC to active promoters depends on PAF1c and, conversely, PAF1c is required for MYC-dependent pause release. Upon binding, PAF1c is rapidly transferred from MYC onto RNAPII and this transfer is driven by the HUWE1 ubiquitin ligase. Both MYC and HUWE1 globally control histone H2B ubiquitylation, which promotes transcriptional elongation and alters chromatin structure for double-strand break repair. Consistently, MYC suppresses the accumulation of double-strand breaks at promoters in response to topoisomerase II inhibition. While depletion of PAF1c has only minor effects on MYC-dependent gene expression, MYC induces rampant transcription-dependent DNA damage in PAF1c-depleted cells. We propose that the HUWE1-dependent transfer of PAF1c from MYC onto RNAPII is critical for absorbing the topological stress accompanied with deregulated and oncogenic transcription.
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