ArticleCell death and differentiation2017
A defective dNTP pool hinders DNA replication in cell cycle-reactivated terminally differentiated muscle cells.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Skeletal muscle dedifferentiation requires centrosomes.NPJ Regenerative medicine · 2026Article
- Cryptic DNA sequences encode a temperature sensor to regulate mitochondrial suicide during neuronal differentiation.Cell communication and signaling : CCS · 2026Article
- Structural obstruction to full DNA replication in terminally differentiated skeletal muscle cells.EMBO reports · 2025Article
- Increasing intracellular dNTP levels improves prime editing efficiency.Nature biotechnology · 2025Article
- Whole transcriptome profiling reveals a lncMDP1 that regulates myogenesis by adsorbing miR-301a-5p targeting CHAC1.Communications biology · 2024Article
- Metabolic clogging of mannose triggers dNTP loss and genomic instability in human cancer cells.eLife · 2023Article
- dNTPpoolDB: a manually curated database of experimentally determined dNTP pools and pool changes in biological samples.Nucleic acids research · 2022Article
- Still no Rest for the Reductases: Ribonucleotide Reductase (RNR) Structure and Function: An Update.Sub-cellular biochemistry · 2022Review
- Ferroportin depletes iron needed for cell cycle progression in head and neck squamous cell carcinoma.Frontiers in oncology · 2022Article
- Replication Stress, Genomic Instability, and Replication Timing: A Complex Relationship.International journal of molecular sciences · 2021Review
- Skeletal Muscle Is an Antigen Reservoir in Integrase-Defective Lentiviral Vector-Induced Long-Term Immunity.Molecular therapy. Methods & clinical development · 2020Article
- The role of dNTP metabolites in control of the embryonic cell cycle.Cell cycle (Georgetown, Tex.) · 2019Review
- Interferon γ and α Have Differential Effects on SAMHD1, a Potent Antiviral Protein, in Feline Lymphocytes.Viruses · 2019Article
- SAMHD1: Recurring roles in cell cycle, viral restriction, cancer, and innate immunity.Autoimmunity · 2018Review
- Targeting Nucleotide Biosynthesis: A Strategy for Improving the Oncolytic Potential of DNA Viruses.Frontiers in oncology · 2017Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Terminally differentiated cells are defined by their inability to proliferate. When forced to re-enter the cell cycle, they generally cannot undergo long-term replication. Our previous work with myotubes has shown that these cells fail to proliferate because of their intrinsic inability to complete DNA replication. Moreover, we have reported pronounced modifications of deoxynucleotide metabolism during myogenesis. Here we investigate the causes of incomplete DNA duplication in cell cycle-reactivated myotubes (rMt). We find that rMt possess extremely low levels of thymidine triphosphate (dTTP), resulting in very slow replication fork rates. Exogenous administration of thymidine or forced expression of thymidine kinase increases deoxynucleotide availability, allowing extended and faster DNA replication. Inadequate dTTP levels are caused by selective, differentiation-dependent, cell cycle-resistant suppression of genes encoding critical synthetic enzymes, chief among which is thymidine kinase 1. We conclude that lack of dTTP is at least partially responsible for the inability of myotubes to proliferate and speculate that it constitutes an emergency barrier against unwarranted DNA replication in terminally differentiated cells.
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Registered trials
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