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Effect of depletion of IntS4, IntS6, mts, or Pp2A-29B on gene expression in Drosophila DL1 cells

ABSTRACT: To investigate the effect of depletion of Integrator complex subunits IntS4, IntS6, mts, or Pp2A-29B on gene expression

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE223974 | GEO | 2023/11/10

REPOSITORIES: GEO

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Effect of depletion of IntS4, IntS6, mts, or Pp2A-29B on gene expression in Drosophila DL1 cells

Project description:Effect of depletion of IntS4, IntS6, mts, or Pp2A-29B on gene expression in Drosophila DL1 cells

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A PP2A-Integrator complex fine-tunes transcription by opposing CDK9 [3UTR-seq]

Project description:Gene expression by RNA Polymerase II (RNAPII) is tightly controlled by Cyclin-dependent kinases (CDKs) at discrete checkpoints during the transcription cycle. The RNAPII pausing checkpoint, engaged after transcription initiation, is controlled by CDK9 to regulate transcription in metazoans. We discovered that CDK9-mediated RNAPII pause-release is functionally opposed by a protein phosphatase 2A (PP2A) complex. PP2A dynamically competes for key CDK9 substrates, DSIF and RNAPII-CTD, and is recruited to transcription pausing sites by the Integrator complex subunit INTS6. INTS6 depletion confers resistance to CDK9 inhibition in a variety of normal and tumor cell lines. Loss of INTS6 abolishes the Integrator-PP2A association leading to unrestrained CDK9 activity, which amplifies transcriptional responses. Pharmacological PP2A activation synergizes with CDK9 inhibition to kill MLL-rearranged leukemias and solid tumors and provide therapeutic benefit in vivo. These data demonstrate that f inely-tuned gene expression relies on the balance of kinase and phosphatase activity at the pausing checkpoint.

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A PP2A-Integrator complex fine-tunes transcription by opposing CDK9 [ChIP-seq]

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A PP2A-Integrator complex fine-tunes transcription by opposing CDK9 [4sU-seq]

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A PP2A-Integrator complex fine-tunes transcription by opposing CDK9

Project description:Gene expression by RNA Polymerase II (RNAPII) is tightly controlled by Cyclindependent kinases (CDKs) at discrete checkpoints during the transcription cycle. The RNAPII pausing checkpoint, engaged after transcription initiation, is controlled by CDK9 to regulate transcription in metazoans. We discovered that CDK9-mediated RNAPII pause-release is functionally opposed by a protein phosphatase 2A (PP2A) complex. PP2A dynamically competes for key CDK9 substrates, DSIF and RNAPIICTD, and is recruited to transcription pausing sites by the Integrator complex subunit INTS6. INTS6 depletion confers resistance to CDK9 inhibition in a variety of normal and tumor cell lines. Loss of INTS6 abolishes the Integrator-PP2A association leading to unrestrained CDK9 activity, which amplifies transcriptional responses. Pharmacological PP2A activation synergizes with CDK9 inhibition to kill MLLrearranged leukemias and solid tumors and provide therapeutic benefit in vivo. These data demonstrate that finely-tuned gene expression relies on the balance of kinase and phosphatase activity at the pausing checkpoint.

2022-08-12 | PXD022962 | Pride

A PP2A-Integrator complex fine-tunes transcription by opposing CDK9

Project description:In this study, we discovered that CDK9-mediated, RNAPII-driven transcription is functionally opposed by a protein phosphatase 2A (PP2A) complex that is recruited to transcription sites by the Integrator complex subunit INTS6. PP2A dynamically antagonises phosphorylation of key CDK9 substrates including DSIF and RNAPII-CTD. Loss of INTS6 results in resistance to tumor cell death mediated by CDK9 inhibition, decreased turnover of CDK9 phospho-substrates and amplification of acute cell growth and pro-inflammatory transcriptional responses. Pharmacological PP2A activation synergizes with CDK9 inhibition to kill both leukemic and solid tumor cells, providing therapeutic benefit in vivo. These data demonstrate that finely-tuned gene expression relies on the balance of kinase and phosphatase activity throughout the transcription cycle.

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INTS6 controls DNA:RNA hybrids autoregulation at double-strand break through Senataxin

Project description:The fidelity of transcription is essential for genome stability, especially when DNA damage happens. However, how the transcription cycle is regulated remains unknown. Here, we found that INTS6 is a fundamental player, which recruits PP2A to double-strand breaks (DSBs) and functions together with senataxin (SETX). The in-depth insight of ChromeRNA-seq shows that INTS6 is not only involved in global transcription termination but also the de novo transcription termination. Therefore, INTS6 is a great target for future translational studies.

2024-10-18 | GSE246729 | GEO

Effect of overexpression of IntS6 and IntS12 on gene expression in Drosophila DL1 cells

Project description:To investigate the effect of IntS6 or IntS12 overexpression on gene expression

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A PP2A-Integrator complex regulates transcriptional pause-release by functionally opposing CDK9

Project description:We investigated the function of the Integrator Complex and PP2A during transcription.

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Integrator-PP2A complex dephosphorylates the C-terminal repeat domain of RNA Polymerase II

Project description:The phosphorylation and dephosphorylation of transcription machinery are essential for the precise control of gene expression. A non-canonical protein phosphatase 2A (PP2A) holoenzyme (denoted INTAC), in which the 14-subunit Integrator recruits RNA polymerase II (Pol II) and the PP2A core enzyme dephosphorylates the C-terminal repeat domain (CTD) of Pol II at Serine-5 and Serine-2.

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