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Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells

ABSTRACT: To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE41242 | GEO | 2012/10/18

SECONDARY ACCESSION(S): PRJNA176305

REPOSITORIES: GEO

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Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells

Project description:To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection Drosophila cells were treated with Bgal or Cdk9 and infected with VSV (MOI 10) for 4 hours, in two independent biological replicates. Total RNA was isolated using Trizol and microarray experiments were performed at the University of Pennsylvania Microarray Facility (U. Penn MF) following directions according to the manufacturerM-bM-^@M-^Ys protocol (Affymetrix). In brief, 100 ng RNA were amplified with the Ovation RNA Amplification System v2 (NuGen), the Encore Biotin Module (NuGen) was used for fragmentation and labeling, Protocol FS450 002 was used for hybridization, washing, and staining. Images were scanned using the GeneChipM-BM-. Scanner 3000 and image analysis was performed using the AffymetrixM-BM-. GeneChipM-BM-. Command ConsoleM-BM-. Software (AGCC).

2012-10-18 | E-GEOD-41242 | biostudies-arrayexpress

Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection

Project description:Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells

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Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection

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Targeting CDK9 Reactivates Epigenetically Silenced Genes in Cancer

Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation by promoting RNAPII pause release. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition dephosphorylates the SWI/SNF protein SMARCA4 and represses HP1α expression, both of which contribute to gene reactivation. Based on gene activation, we developed the highly selective and potent CDK9 inhibitor MC180295 (IC50 =5.1nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition sensitizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.

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Project description:Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells

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Influences of CDK9 on gene expressions

Project description:To understand better the contribution of CDK9 in P. gingivalis-stimulated gene expression, gene chips were performed. Lentiviral vectors carrying CDK9 shRNA or not were transfected into cells for 96 hours, with the assist of Envirus. NC group was transfected with non-targeting scramble and stimulated with PBS. NC and Pg group was transfected with non-targeting scramble and stimulated with P. gingivalis. CDK9 shRNA group was transfected with CDK9 shRNA and stimulated with PBS. CDK9 shRNA and Pg group was transfected with CDK9 shRNA and stimulated with P. gingivalis.

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RIP- seq identified the interacted RNAs of SAFA with or without VSV infection

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Argonaute2 attenuates active transcription by limiting RNA Polymerase II elongation in Drosophila melanogaster [ChIPseq-CDK9]

Project description:Increasing lines of evidence support that Argonaute2 (AGO2) harbors several nuclear functions in metazoa. In particular, Drosophila AGO2 modulates transcription of developmentally regulated genes; however, the molecular mechanisms behind AGO2 recruitment into chromatin and its function in transcription have not been deeply explored. In this study, we show that Drosophila AGO2 chromatin association depends on active transcription. In order to gain insight into how AGO2 controls transcription, we performed differential ChIP-seq analysis for RNA Polymerase II (Pol II) upon depletion of AGO2. Interestingly, we find specific accumulation of the elongating but not initiating form of Pol II after AGO2 knockdown, suggesting that AGO2 impairs transcription elongation. Finally, AGO2 also affects Negative Elongation Factor (CDK9) chromatin association but not the Cyclin Dependent Kinase 9 (CDK9). Altogether, these results provide key insights into the molecular role of AGO2 in attenuating elongation of certain actively transcribed genes.

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