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CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression (3' RNA)

ABSTRACT: CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression (3' RNA)

PROVIDER: PRJNA491605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7865850.fastq.gz	Fastqsanger.gz
	SRR7865851.fastq.gz	Fastqsanger.gz
	SRR7865852.fastq.gz	Fastqsanger.gz
	SRR7865853.fastq.gz	Fastqsanger.gz
	SRR7865854.fastq.gz	Fastqsanger.gz

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CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression (nuclear RNA)

Project description:In this study we characterized the importance of CDK12-kinase activity in cell cycle regulation, using CDK12 anolog-sentive cells. Inhibition of analog-sensitive CDK12 reveals its catalytic activity is necessary for optimal G1/S progression. Mechanistically, CDK12 regulates transcription of core DNA replication genes and affects timely assembly of pre-replication DNA complex on chromatin. We have performed 3’-end RNA-sequencing after CDK12 inhibition and identified that the expression of core DNA replication genes were affected. To investigate further, we carried out nuclear RNA-seq coupled with ChIP-seq, and demonstrated that CDK12 regulates RNAPII processivity of core DNA replication genes and optimal G1/S progression.

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Project description:CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression

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CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression (nuclear RNA)

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CDK13 cooperates with CDK12 to control global RNA polymerase II processivity

Project description:The RNA polymerase II (POLII) driven transcription cycle is tightly regulated at distinct checkpoints through cyclin dependent kinases (CDKs) and their cognate Cyclins. The molecular events underpinning transcriptional elongation and processivity and CDK-Cyclins involved remain poorly understood. Using CRISPR-CAS9 homology-directed-repair we generated analog-sensitive-kinase variants of CDK12 and CDK13 to probe their individual and shared biological and molecular roles. Single inhibition of CDK12 or CDK13 induced transcriptional responses associated with DNA-damage and cellular growth signaling pathways respectively, with minimal effects on cell viability. In contrast, dual-kinase inhibition potently induced cell death, which was associated with extensive genome-wide transcriptional changes including wide-spread use of alternative 3’ polyadenylation sites. At the molecular level dual-kinase inhibition resulted in the loss of POLII CTD phosphorylation and greatly reduced POLII elongation rates and processivity. These data define significant redundancy between CDK12 and CDK13, and identify both as fundamental regulators of global POLII processivity and transcription elongation.

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CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression

Project description:This SuperSeries is composed of the SubSeries listed below.

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