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Mol Cell. 2015 Nov 5;60(3):435-45. doi: 10.1016/j.molcel.2015.09.021.

Mitotic Transcriptional Activation: Clearance of Actively Engaged Pol II via Transcriptional Elongation Control in Mitosis.

Author information

1
Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, 320 E. Superior Street, Chicago, IL 60611, USA; Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA.
2
Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, 320 E. Superior Street, Chicago, IL 60611, USA.
3
Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA.
4
Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA; Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.
5
Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, 320 E. Superior Street, Chicago, IL 60611, USA; Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, 320 E. Superior Street, Chicago, IL 60611, USA. Electronic address: ash@northwestern.edu.

Abstract

Although it is established that some general transcription factors are inactivated at mitosis, many details of mitotic transcription inhibition (MTI) and its underlying mechanisms are largely unknown. We have identified mitotic transcriptional activation (MTA) as a key regulatory step to control transcription in mitosis for genes with transcriptionally engaged RNA polymerase II (Pol II) to activate and transcribe until the end of the gene to clear Pol II from mitotic chromatin, followed by global impairment of transcription reinitiation through MTI. Global nascent RNA sequencing and RNA fluorescence in situ hybridization demonstrate the existence of transcriptionally engaged Pol II in early mitosis. Both genetic and chemical inhibition of P-TEFb in mitosis lead to delays in the progression of cell division. Together, our study reveals a mechanism for MTA and MTI whereby transcriptionally engaged Pol II can progress into productive elongation and finish transcription to allow proper cellular division.

PMID:
26527278
PMCID:
PMC5548174
DOI:
10.1016/j.molcel.2015.09.021
[Indexed for MEDLINE]
Free PMC Article

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