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RNA-Seq for validating the RNA expression of wild type and analog sensitive CDK12 and CDK13 in analog sensitive MV4;11 cell lines that generated by CRISPR HDR

ABSTRACT: We used Poly-A enriched RNA-Seq to validate CDK12, CDK13 anlalog senstive mutationsand their expression level in the cell lines that has analog sensitive mutations that were introduced by CRISPR HDR

ORGANISM(S): Homo sapiens

PROVIDER: GSE141366 | GEO | 2020/04/29

REPOSITORIES: GEO

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Transcriptome wide analysis of differential gene expression and polyadenylation site usages caused by inhibition of CDK12 and/or CDK13 in MV4;11 cells (3’ Quant-seq)

Project description:We used 3' RNA-Seq to determine the effects of analog senstive CDK12, CDK13 and dual inhibition on gene expression and polyadenatltion site usages, and to test the redundancy between CDK12 and CDK13 in maintaining global transcrition on the tramcrotpomte level.

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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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Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors [ChIP-Seq]

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