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Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [ChIP-chip]

ABSTRACT: The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex. Two independent immunoprecipitations were done for HA-tagged Cdk11 and each biological replicate was hybridized in duplicate on Agilent arrays using input DNA as the reference channel.

ORGANISM(S): Schizosaccharomyces pombe

SUBMITTER: Harm Bakel

PROVIDER: E-GEOD-37961 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cdk11-cyclinL controls the assembly of the RNA polymerase II mediator complex.

Drogat Julie J Migeot Valérie V Mommaerts Elise E Mullier Caroline C Dieu Marc M van Bakel Harm H Hermand Damien D

Cell reports 20121101 5

The large Mediator (L-Mediator) is a general coactivator of RNA polymerase II transcription and is formed by the reversible association of the small Mediator (S-Mediator) and the kinase-module-harboring Cdk8. It is not known how the kinase module association/dissociation is regulated. We describe the fission yeast Cdk11-L-type cyclin pombe (Lcp1) complex and show that its inactivation alters the global expression profile in a manner very similar to that of mutations of the kinase module. Cdk11 i ...[more]

PMID: 23122962

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Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [expression]

Project description:The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex. Total RNA was isolated from two biological replicates for all conditions, and each biological replicate was hybridized in duplicate on Agilent arrays (dye-swap).

2014-07-11 | E-GEOD-37960 | biostudies-arrayexpress

Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [ChIP-chip]

2014-07-11 | GSE37961 | GEO

Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [expression]

2014-07-11 | GSE37960 | GEO

Sexual differentiation controlled by RNA polymerase II CTD phosphorylation on serine 2

Project description:The switch from cellular proliferation to differentiation occurs to a large extend through specific programs of gene expression. In fission yeast, the high-mobility-group transcription factor Ste11 is the master regulator of sexual differentiation. ste11 is induced by environmental conditions, mostly nitrogen starvation, leading to mating and meiosis 1. We have used ChIP-chip and gene expression profiling to show that CDK-dependent phosphorylation of serine 2 in the C-terminal domain (CTD) of the largest subunit of the RNA polymerase II (PolII) holoenzyme plays a critical role in the induction of ste11 transcription during sexual differentiation while it has a minor impact on gene expression during vegetative growth. Moreover, we demonstrate that both the recruitment of the CTD serine 2 kinase and the phosphorylation event initiate at the promoter region of ste11 in contrast to the classical case where serine 2 phosphorylation occurs across the coding region 2. In the absence of CTD serine 2 phosphorylation, both PolII occupancy at the ste11 locus, and ste11 expression are impaired. This results in sterility that is rescued when ste11 is expressed from the canonical adh promoter. We conclude that a modification of the RNA polymerase II holoenzyme plays a specific and pivotal role in the sexual differentiation. For the ChIP-chip experiments, 3-4 biological replicates were performed for each tagged protein of interest. For the expression experiments, two biological samples were hybridized for each mutant strain (replicates 1 and 2), with two dye-swap technical replicates per sample (replicates 3 and 4).

2010-01-01 | E-GEOD-16498 | biostudies-arrayexpress

A study of Mediator subunit enhancer-promoter binding

Project description:Mediator is a transcriptional co-activator recruited to enhancers by DNA-binding activators, and it also interacts with RNA polymerase (Pol) II as part of the preinitiation complex (PIC). We demonstrate that a single Mediator complex associates with the enhancer and core promoter in vivo, indicating that it can physically bridge these transcriptional elements. However, the Mediator kinase module associates strongly with the enhancer, but not with the core promoter, and it dissociates from the enhancer upon depletion of the TFIIH kinase. Severing the kinase module from Mediator by removing the connecting subunit Med13 does not affect Mediator association at the core promoter, but increases occupancy at enhancers. Thus, Mediator undergoes a compositional change in which the kinase module, recruited via Mediator to the enhancer, dissociates from Mediator to permit association with Pol II and the PIC. As such, Mediator acts as a dynamic bridge between the enhancer and core promoter.

2016-10-31 | GSE82082 | GEO

Structural basis of the human transcriptional Mediator complex modulated by its dissociable Kinase module

Project description:The Mediator complex consists of a Core and a dissociable Kinase module. This project is to understand the binding mode between the Core and Kinase module. Both Mediator complex and its Kinase module were individually crosslinked and analyzed by XL-MS.

2024-11-21 | PXD044328 | Pride

CDK11 loss induces cell cycle dysfunction and death of BRAF and NRAS melanoma cells

Project description:Cyclin dependent kinase 11 (CDK11) is a protein kinase that regulates RNA transcription, pre-mRNA splicing, mitosis, and cell death. Targeting of CDK11 expression levels is effective in the experimental treatment of breast and other cancers, but these data are lacking in melanoma. To understand CDK11 function in melanoma, we evaluated protein and RNA levels of CDK11, Cyclin L1 and Cyclin L2 in benign melanocytes and BRAF- as well as NRAS-mutant melanoma cell lines. We investigated the effectiveness of reducing expression of this survival kinase using RNA interference on viability, clonal survival, and tumorsphere formation in melanoma cell lines. We examined the impact of CDK11 loss in BRAF-mutant melanoma on more than 700 genes important in cancer signaling pathways. Follow-up analysis evaluated how CDK11 loss alters cell cycle function in BRAF- and NRAS-mutant melanoma cells. We present data on CDK11, CCNL1 and CCNL2 mRNA expression in melanoma patients, including prognosis for survival. In sum, we found that CDK11 is necessary for melanoma cell survival, and a major impact of CDK11 loss in melanoma is to cause disruption of the cell cycle distribution with accumulation of G1- and loss of G2/M-phase cancer cells.

2019-05-08 | GSE128693 | GEO

The Pol II Pre-Initiation Complex (PIC) Influences Mediator Binding but Not Promoter-Enhancer Looping [RNA-seq]

Project description:Knowledge of how Mediator and TFIID crosstalk contributes to promoter-enhancer (P-E) communication is important for elucidating the mechanism of enhancer function. We conducted an shRNA knockdown screen in murine embryonic stem cells to identify the functional overlap between Mediator and TFIID subunits on gene expression. Auxin-inducible degrons were constructed for TAF12 and MED4, the subunits eliciting the greatest overlap. Degradation of TAF12 led to a dramatic genomewide decrease in gene expression accompanied by destruction of TFIID, loss of Pol II pre-initiation complex (PIC) at the promoter, and significantly decreased Mediator binding to promoters and enhancers. Interestingly, loss of the PIC elicited only a mild effect on P-E looping by Promoter Capture Hi-C (PCHi-C). Degradation of MED4 had a minor effect of Mediator integrity but led to a consistent 2-fold loss in gene expression, decreased binding of Pol II to Mediator, and decreased recruitment of Pol II to the promoters, but no effect on the other PIC components. PCHi-C revealed no consistent effect of Med4 degradation on P-E looping. Collectively, our data show that TAF12 and MED4 contribute mechanistically in different ways to P-E communication but neither factor appears to directly control P-E looping, thereby dissociating P-E communication from physical looping.

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The Pol II Pre-Initiation Complex (PIC) Influences Mediator Binding but Not Promoter-Enhancer Looping [ChIP-seq]

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