Translate to divide: сontrol of the cell cycle by protein synthesis
Open accessAbstract
Protein synthesis underpins much of cell growth and, consequently, cell multiplication. Understanding how proliferating cells commit and progress into the cell cycle requires knowing not only which proteins need to be synthesized, but also what determines their rate of synthesis during cell division.
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Inhibition of rRNA production can halt cell cycle activity with accompanying decreases in cell size.
“inhibition of rRNA production can halt cell cycle activity (Polymenis and Aramayo, 2015) with accompanying decreases in cell size”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Polymenis and Aramayo, 2015
In “INITIATE TO START?” (page unavailable), the table lists RNA polymerase I subunits with G1 arrest, supporting the claim that disrupting rRNA production can halt cell-cycle progression in yeast. “RIBOSOME MAKES PROTEIN MAKES CELLS?” (page unavailable) reports smaller cells for some ribosomal-protein mutants, but does not establish that inhibiting rRNA production itself causes the accompanying decrease in cell size. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn eukaryotic cells, deletion and/or knockdown of key genes regulating protein synthesis, such as eIFs, results in delayed cell cycle entry.
“Hence, in eukaryotic cells, deletion and/or knockdown of key genes regulating protein synthesis, such as translation elongation initiation factors (eIFs), several of which are repressed by IL-1 in our dataset, results in delayed cell cycle entry (Polymenis and Aramayo, 2015).”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Polymenis and Aramayo, 2015
The “INITIATE TO START?” section (page unavailable) reports that inhibiting several eIFs causes G1 arrest and prevents initiation of a new round of division in yeast. This supports the knockdown-like part of the claim, but the cited genetic evidence is in yeast; it does not establish the stated result generally across eukaryotic cells or specifically for eIF gene deletion. (LLM, conf=0.86)
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Cites
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Tuller, T., Waldman, Y. Y., Kupiec, M., & Ruppin, E. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0909910107 · Cited by 584 · see citing works
A comprehensive, quantitative, and genome-wide model of translation
Siwiak, M., & Zielenkiewicz, P. (2010) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1000865 · Cited by 93 · see citing works
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Wallace, E. W. J., Airoldi, E. M., & Drummond, D. A. (2013) · Molecular Biology and Evolution · doi:10.1093/molbev/mst051 · Cited by 48 · see citing works
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“Hence, in eukaryotic cells, deletion and/or knockdown of key genes regulating protein synthesis, such as translation elongation initiation factors (eIFs), several of which are repressed by IL-1 in our dataset, results in delayed cell cycle entry (Polymenis and Aramayo, 2015).”
Background
- Authors
- Department of Biochemistry and Biophysics, T. A. U., Polymenis, M., Aramayo, R., & Department of Biology, T. A. U.
- Affiliations
- Texas A&M University (US)
- Corresponding author
- Polymenis, Michael
- Aramayo, Rodolfo
- Venue
- Microbial Cell
- Publisher
- Shared Science Publishers OG
- Published
- 2015-04-06
- Volume
- 2
- Issue
- 4
- Pages
- 94-104
- ISSN
- 2311-2638 (ISSN-L)
- PMC
- PMC5348972
- OpenAlex
- W2104240441
- Cited by
- 91
- References
- 5
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 8 · 2023: 8 · 2022: 8 · 2021: 6 · 2020: 21 · 2019: 9 · 2018: 4 · 2017: 8 · 2016: 3
- FWCI
- 0.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Microbial Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- OakTrust (Texas A&M University Libraries) (submittedVersion, cc-by)
- Funders
- National Science Foundation (0818248)
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM058770)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cell cycle regulation, protein synthesis, cell proliferation, cell division, cell growth, translation rate, protein synthesis rate
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