Cdk9 regulates a promoter-proximal checkpoint to modulate RNA polymerase II elongation rate in fission yeast

Gregory T. Booth, Pabitra K. Parua, Miriam Sansó, Robert P. Fisher and John T. Lis ()
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Gregory T. Booth: Cornell University
Pabitra K. Parua: Icahn School of Medicine at Mount Sinai
Miriam Sansó: Icahn School of Medicine at Mount Sinai
Robert P. Fisher: Icahn School of Medicine at Mount Sinai
John T. Lis: Cornell University

Nature Communications, 2018, vol. 9, issue 1, 1-10

Abstract: Abstract Post-translational modifications of the transcription elongation complex provide mechanisms to fine-tune gene expression, yet their specific impacts on RNA polymerase II regulation remain difficult to ascertain. Here, in Schizosaccharomyces pombe, we examine the role of Cdk9, and related Mcs6/Cdk7 and Lsk1/Cdk12 kinases, on transcription at base-pair resolution with Precision Run-On sequencing (PRO-seq). Within a minute of Cdk9 inhibition, phosphorylation of Pol II-associated factor, Spt5 is undetectable. The effects of Cdk9 inhibition are more severe than inhibition of Cdk7 and Cdk12, resulting in a shift of Pol II toward the transcription start site (TSS). A time course of Cdk9 inhibition reveals that early transcribing Pol II can escape promoter-proximal regions, but with a severely reduced elongation rate of only ~400 bp/min. Our results in fission yeast suggest the existence of a conserved global regulatory checkpoint that requires Cdk9 kinase activity.

Date: 2018
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DOI: 10.1038/s41467-018-03006-4

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