Functional interplay between MSL1 and CDK7 controls RNA polymerase II Ser5 
phosphorylation

Chlamydas, Sarantis; Holz, Herbert; Samata, Maria; Chelmicki, Tomasz; Georgiev, Plamen; Pelechano, Vicent; Dündar, Friederike; Dasmeh, Pouria; Mittler, Gerhard; Tavares Cadete, Filipe; Ramirez, Fidel; Conrad, Thomas; Wei, Wu; Raja, Sunil; Manke, Thomas; Luscombe, Nicholas M.; Steinmetz, Lars M.; Akhtar, Asifa

doi:10.1038/nsmb.3233

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Functional interplay between MSL1 and CDK7 controls RNA polymerase II Ser5 phosphorylation

MPS-Authors

Chlamydas, Sarantis
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Holz, Herbert
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Samata, Maria
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
University of Freiburg, Faculty of Biology;

Chelmicki, Tomasz
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Georgiev, Plamen
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Dündar, Friederike
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
University of Freiburg, Faculty of Biology;

Dasmeh, Pouria
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Mittler, Gerhard
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ramirez, Fidel
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Conrad, Thomas
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Raja, Sunil
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Manke, Thomas
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons198888

Akhtar, Asifa
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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https://www.nature.com/articles/nsmb.3233
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Citation

Chlamydas, S., Holz, H., Samata, M., Chelmicki, T., Georgiev, P., Pelechano, V., et al. (2016). Functional interplay between MSL1 and CDK7 controls RNA polymerase II Ser5 phosphorylation. Nature Structural and Molecular Biology, 23, 580-589. doi:10.1038/nsmb.3233.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002C-A8D5-0

Abstract

Proper gene expression requires coordinated interplay among transcriptional coactivators, transcription factors and the general transcription machinery. We report here that MSL1, a central component of the dosage compensation complex in Drosophila melanogaster and Drosophila virilis, displays evolutionarily conserved sex-independent binding to promoters. Genetic and biochemical analyses reveal a functional interaction of MSL1 with CDK7, a subunit of the Cdk-activating kinase (CAK) complex of the general transcription factor TFIIH. Importantly, MSL1 depletion leads to decreased phosphorylation of Ser5 of RNA polymerase II. In addition, we demonstrate that MSL1 is a phosphoprotein, and transgenic flies expressing MSL1 phosphomutants show mislocalization of the histone acetyltransferase MOF and histone H4 K16 acetylation, thus ultimately causing male lethality due to a failure of dosage compensation. We propose that, by virtue of its interaction with components of the general transcription machinery, MSL1 exists in different phosphorylation states, thereby modulating transcription in flies.