ArticleNucleic acids research2018
Cdk1 gates cell cycle-dependent tRNA synthesis by regulating RNA polymerase III activity.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
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- Coupling Between Cell Cycle Progression and the Nuclear RNA Polymerases System.Frontiers in molecular biosciences · 2021Review
- Bioinformatics analysis of BUB1 expression and gene regulation network in lung adenocarcinoma.Translational cancer research · 2020Article
- Determinants of Replication-Fork Pausing at tRNA Genes inGenetics · 2020Article
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- Bioinformatics Identification of the Expression and Clinical Significance of E2F Family in Endometrial Cancer.Frontiers in genetics · 2020Article
- Coupling of RNA polymerase III assembly to cell cycle progression in Saccharomyces cerevisiae.Cell cycle (Georgetown, Tex.) · 2019Article
- Expression and gene regulation network ofAging · 2019Article
- A cell competition-based small molecule screen identifies a novel compound that induces dual c-Myc depletion and p53 activation.The Journal of biological chemistryArticle
- Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
tRNA genes are transcribed by RNA polymerase III (RNAPIII). During recent years it has become clear that RNAPIII activity is strictly regulated by the cell in response to environmental cues and the homeostatic status of the cell. However, the molecular mechanisms that control RNAPIII activity to regulate the amplitude of tDNA transcription in normally cycling cells are not well understood. Here, we show that tRNA levels fluctuate during the cell cycle and reveal an underlying molecular mechanism. The cyclin Clb5 recruits the cyclin dependent kinase Cdk1 to tRNA genes to boost tDNA transcription during late S phase. At tDNA genes, Cdk1 promotes the recruitment of TFIIIC, stimulates the interaction between TFIIIB and TFIIIC, and increases the dynamics of RNA polymerase III in vivo. Furthermore, we identified Bdp1 as a putative Cdk1 substrate in this process. Preventing Bdp1 phosphorylation prevented cell cycle-dependent recruitment of TFIIIC and abolished the cell cycle-dependent increase in tDNA transcription. Our findings demonstrate that under optimal growth conditions Cdk1 gates tRNA synthesis in S phase by regulating the RNAPIII machinery, revealing a direct link between the cell cycle and RNAPIII activity.
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