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Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [CDK9-chIP-seq]

ABSTRACT: To investigate changes in p-TEFb distribution in response to SF3B1 mutations, we peformed ChIP-seq using antibody against the CDK9 component of pTEFb in K562 cells (wild type and SF3B1K700E mutant) at 4 days after mutant allele expression We then performed coverage plot analysis using data obtained from ChIP-seq from IP and Input fractions to investigate CDK9 distribution changes

ORGANISM(S): Homo sapiens

PROVIDER: GSE225996 | GEO | 2024/03/12

REPOSITORIES: GEO

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Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [NTD-chIP-seq]

Project description:To investigate changes in RNAPII distribution in response to SF3B1 mutations, we peformed ChIP-seq using antibody against N-terminal domain of RNAPII (Pan-Pol2) in K562 cells (wild type and SF3B1K700E mutant) at 4 days after mutant allele expression We then performed coverage plot analysis using data obtained from ChIP-seq to investigate RNAPII distribution changes

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Expression profiling of HeLa cell line treated with CDK9 inhibitor

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. We used microarrays to examine the global impact on gene expression by imhibiting CDK9 at different time durations. HeLa cell lines treated with CDK9 inhibitor at different time points

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Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [Ser5PRNAPII ChIP-Seq]

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Project description:To investigate changes in Pol2 distribution in response to SF3B1 mutations, we peformed ChIP-seq using antibody against Pol2 (both CTD and elongation specific (Ser2P and Ser5p). For the murine model, SF3B1 mutant (and WT counterparts) were treated with tamoxifen daily x 5 days at 5 weeks of age. Mice were euthanized at end of week 7 and bone marrow was harvested to isolate lineage negative cells We then performed coverage plot analysis using data obtained from ChIP-seq from IP fractions to investigate Pol2 distribution changes

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Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism: Pol II occupancy profiling by ChIP-Seq in HeLa cell line in the presence or absence of CDK9 inhibition

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. ChIP-seq of Pol II in HeLa cells before or after i-CDk9 treatment

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