Distinct Cdk9-phosphatase switches act at the beginning and end of elongation by RNA polymerase II.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
28 08 2020
Historique:
received: 11 06 2020
accepted: 10 08 2020
entrez: 30 8 2020
pubmed: 30 8 2020
medline: 18 9 2020
Statut: epublish

Résumé

Reversible phosphorylation of Pol II and accessory factors helps order the transcription cycle. Here, we define two kinase-phosphatase switches that operate at different points in human transcription. Cdk9/cyclin T1 (P-TEFb) catalyzes inhibitory phosphorylation of PP1 and PP4 complexes that localize to 3' and 5' ends of genes, respectively, and have overlapping but distinct specificities for Cdk9-dependent phosphorylations of Spt5, a factor instrumental in promoter-proximal pausing and elongation-rate control. PP1 dephosphorylates an Spt5 carboxy-terminal repeat (CTR), but not Spt5-Ser666, a site between Kyrpides-Ouzounis-Woese (KOW) motifs 4 and 5, whereas PP4 can target both sites. In vivo, Spt5-CTR phosphorylation decreases as transcription complexes pass the cleavage and polyadenylation signal (CPS) and increases upon PP1 depletion, consistent with a PP1 function in termination first uncovered in yeast. Depletion of PP4-complex subunits increases phosphorylation of both Ser666 and the CTR, and promotes redistribution of promoter-proximally paused Pol II into gene bodies. These results suggest that switches comprising Cdk9 and either PP4 or PP1 govern pause release and the elongation-termination transition, respectively.

Identifiants

pubmed: 32859893
doi: 10.1038/s41467-020-18173-6
pii: 10.1038/s41467-020-18173-6
pmc: PMC7455706
doi:

Substances chimiques

Nuclear Proteins 0
Receptors, Neuropeptide Y 0
SUPT5H protein, human 0
Transcriptional Elongation Factors 0
neuropeptide Y4 receptor 55F8T1GN3X
Positive Transcriptional Elongation Factor B EC 2.7.11.-
CDK9 protein, human EC 2.7.11.22
Cyclin-Dependent Kinase 9 EC 2.7.11.22
RNA Polymerase II EC 2.7.7.-

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

4338

Subventions

Organisme : NCI NIH HHS
ID : P30 CA196521
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM127289
Pays : United States

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Auteurs

Pabitra K Parua (PK)

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, USA.

Sampada Kalan (S)

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, USA.

Bradley Benjamin (B)

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, USA.

Miriam Sansó (M)

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, USA.

Robert P Fisher (RP)

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, USA. Robert.fisher@mssm.edu.

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