ArticleProceedings of the National Academy of Sciences of the United States of America2015
CDK1 substitutes for mTOR kinase to activate mitotic cap-dependent protein translation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 141 citations in OpenAlex.
- Mitotic assembly of respiratory supercomplexes ensures accurate cell division and fuels tumor growth.EMBO reports · 2026Article
- Regulation of mRNA decay and translation during the mammalian cell cycle.RNA (New York, N.Y.) · 2026Review
- mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.Science signaling · 2026Article
- CDK1-dependent N-terminal NuMA phosphorylation promotes dynein-dynactin-NuMA assembly for accurate chromosome segregation.Cell reports · 2026Article
- Decreased tRNA abundance contributes to decreased translation elongation rate in a prolonged mitosis.bioRxiv : the preprint server for biology · 2026Article
- Pharmacologic reversion of Merkel cell carcinoma via CBP/p300 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Investigation of the mechanism of Yijing Decoction in the treatment of premature ovarian insufficiency: A network pharmacology study.Biochemistry and biophysics reports · 2025Article
- Upstream open reading frame translation enhances immunogenic peptide presentation in mitotically arrested cancer cells.Nature communications · 2025Article
- Kit-mediated autophagy suppression driven by a viral oncoprotein emerges as a crucial survival mechanism in Merkel cell carcinoma.Autophagy · 2025Article
- CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Review
- mTORC1 activity oscillates throughout the cell cycle, promoting mitotic entry and differentially influencing autophagy induction.Cell reports · 2024Article
- The small tumor antigen of Merkel cell polyomavirus accomplishes cellular transformation by uniquely localizing to the nucleus despite the absence of a known nuclear localization signal.Virology journal · 2024Article
- TORSEL, a 4EBP1-based mTORC1 live-cell sensor, reveals nutrient-sensing targeting by histone deacetylase inhibitors.Cell & bioscience · 2024Article
- TOR regulates variability of protein synthesis rates.The EMBO journal · 2024Article
- Favipiravir, an antiviral drug, in combination with tamoxifen exerts synergistic effect in tamoxifen-resistant breast cancer cells via hTERT inhibition.Scientific reports · 2024Article
- Merkel cell carcinoma: updates in tumor biology, emerging therapies, and preclinical models.Frontiers in oncology · 2024Review
- RNA-seq reveals role of cell-cycle regulating genes in the pathogenicity of a field very virulent infectious bursal disease virus.Frontiers in veterinary science · 2024Article
- The cell cycle and cell size influence the rates of global cellular translation and transcription in fission yeast.The EMBO journal · 2023Article
- Tceal7 Regulates Skeletal Muscle Development through Its Interaction with Cdk1.International journal of molecular sciences · 2023Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mitosis is commonly thought to be associated with reduced cap-dependent protein translation. Here we show an alternative control mechanism for maintaining cap-dependent translation during mitosis revealed by a viral oncoprotein, Merkel cell polyomavirus small T (MCV sT). We find MCV sT to be a promiscuous E3 ligase inhibitor targeting the anaphase-promoting complex, which increases cell mitogenesis. MCV sT binds through its Large T stabilization domain region to cell division cycle protein 20 (Cdc20) and, possibly, cdc20 homolog 1 (Cdh1) E3 ligase adapters. This activates cyclin-dependent kinase 1/cyclin B1 (CDK1/CYCB1) to directly hyperphosphorylate eukaryotic initiation factor 4E (eIF4E)-binding protein (4E-BP1) at authentic sites, generating a mitosis-specific, mechanistic target of rapamycin (mTOR) inhibitor-resistant δ phospho-isoform not present in G1-arrested cells. Recombinant 4E-BP1 inhibits capped mRNA reticulocyte translation, which is partially reversed by CDK1/CYCB1 phosphorylation of 4E-BP1. eIF4G binding to the eIF4E-m(7)GTP cap complex is resistant to mTOR inhibition during mitosis but sensitive during interphase. Flow cytometry, with and without sT, reveals an orthogonal pH3(S10+) mitotic cell population having higher inactive p4E-BP1(T37/T46+) saturation levels than pH3(S10-) interphase cells. Using a Click-iT flow cytometric assay to directly measure mitotic protein synthesis, we find that most new protein synthesis during mitosis is cap-dependent, a result confirmed using the eIF4E/4G inhibitor drug 4E1RCat. For most cell lines tested, cap-dependent translation levels were generally similar between mitotic and interphase cells, and the majority of new mitotic protein synthesis was cap-dependent. These findings suggest that mitotic cap-dependent translation is generally sustained during mitosis by CDK1 phosphorylation of 4E-BP1 even under conditions of reduced mTOR signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.