G 1 cyclin-Cdk promotes cell cycle entry through localized phosphorylation of RNA polymerase II

Cell division is thought to be initiated by cyclin-dependent kinases (Cdks) inactivating key transcriptional inhibitors. In budding yeast, the G cyclin Cln3-Cdk1 complex is thought to directly phosphorylate the Whi5 protein, thereby releasing the transcription factor SBF and committing cells to divi...

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Published in:Science (American Association for the Advancement of Science) 2021-10, Vol.374 (6565), p.347-351
Main Authors: Kõivomägi, Mardo, Swaffer, Matthew P, Turner, Jonathan J, Marinov, Georgi, Skotheim, Jan M
Format: Article
Language:English
Subjects:
CDC28 Protein Kinase, S cerevisiae - genetics
CDC28 Protein Kinase, S cerevisiae - metabolism
Cell Division - genetics
Cell Division - physiology
Cyclins - genetics
Cyclins - metabolism
G1 Phase - genetics
G1 Phase - physiology
Gene Expression Regulation, Fungal
Phosphorylation
Promoter Regions, Genetic
Protein Domains
Repressor Proteins - metabolism
RNA Polymerase II - chemistry
RNA Polymerase II - metabolism
Saccharomyces cerevisiae - cytology
Saccharomyces cerevisiae - metabolism
Saccharomyces cerevisiae - physiology
Saccharomyces cerevisiae Proteins - chemistry
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - metabolism
Transcription Factors - metabolism
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Summary:Cell division is thought to be initiated by cyclin-dependent kinases (Cdks) inactivating key transcriptional inhibitors. In budding yeast, the G cyclin Cln3-Cdk1 complex is thought to directly phosphorylate the Whi5 protein, thereby releasing the transcription factor SBF and committing cells to division. We report that Whi5 is a poor substrate of Cln3-Cdk1, which instead phosphorylates the RNA polymerase II subunit Rpb1’s C-terminal domain on S of its heptapeptide repeats. Cln3-Cdk1 binds SBF-regulated promoters and Cln3’s function can be performed by the canonical S kinase Ccl1-Kin28 when synthetically recruited to SBF. Thus, we propose that Cln3-Cdk1 triggers cell division by phosphorylating Rpb1 at SBF-regulated promoters to promote transcription. Our findings blur the distinction between cell cycle and transcriptional Cdks to highlight the ancient relationship between these two processes.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.aba5186