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Transcriptional elongation control of hypoxic response and therapeutic approaches

ABSTRACT: Transcriptional elongation control of hypoxic response and therapeutic approaches

PROVIDER: PRJNA1024499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26292500_1.fastq.gz	Fastqsanger.gz
	SRR26292500_2.fastq.gz	Fastqsanger.gz
	SRR26292600_1.fastq.gz	Fastqsanger.gz
	SRR26292600_2.fastq.gz	Fastqsanger.gz
	SRR26292501_1.fastq.gz	Fastqsanger.gz

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Transcriptional elongation control of hypoxic response and therapeutic approaches

Project description:The release of paused RNA polymerase II (RNAPII) from promoter-proximal regions is tightly controlled to ensure proper regulation of gene expression. The elongation factor PTEF-b is known to release paused RNAPII via phosphorylation of the RNAPII C-terminal domain by its cyclin-dependent kinase component, CDK9. However, the signal and stress-specific roles of the various RNAPII-associated macromolecular complexes containing PTEF-b/CDK9 are not yet clear. Here, we identify and characterize the CDK9 complex required for transcriptional response to hypoxia. Contrary to previous reports, our data indicate that a CDK9 complex containing BRD4 but not AFF1/4 is essential for this hypoxic stress response. We demonstrate that BRD4 bromodomains (BET) are dispensable for the release of paused RNAPII at hypoxia-activated genes and that BET inhibition by JQ1 is insufficient to impair hypoxic gene response. Mechanistically, we demonstrate that the C-terminal region of BRD4 is required for Polymerase-Associated Factor-1 Complex (PAF1C) recruitment to establish an elongation-competent RNAPII complex at hypoxia-responsive genes. PAF1C disruption using a small-molecule inhibitor (iPAF1C) impairs hypoxia-induced, BRD4-mediated RNAPII release. Together, our results provide insight into potentially targetable mechanisms that control the hypoxia-responsive transcriptional elongation.

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