ArticleCell proliferation2006
Synchronization in the cell cycle by inhibitors of DNA replication induces histone H2AX phosphorylation: an indication of DNA damage.
Article in Cell proliferation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Repair of single-strand breaks during the cell cycle - saturation of repair capacity.Nucleus (Austin, Tex.) · 2026Article
- High resolution profiling of cell cycle-dependent protein and phosphorylation abundance changes in non-transformed cells.Nature communications · 2025Article
- The kinetics of uracil-N-glycosylase distribution inside replication foci.Scientific reports · 2025Article
- A concise guide to fluorescent cell cycle reporters for live-cell imaging.Frontiers in cell and developmental biology · 2025Review
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Cell-cycle arrest at the G1/S boundary enhances transient voltage-gated ion channel expression in human and insect cells.Cell reports methods · 2023Article
- The organizer of chromatin topology RIF1 ensures cellular resilience to DNA replication stress.Life science alliance · 2023Article
- Site-specific decreases in DNA methylation in replicating cells following exposure to oxidative stress.Human molecular genetics · 2023Article
- A mathematical model for cell cycle control: graded response or quantized response.Cell cycle (Georgetown, Tex.) · 2022Article
- Strengths and Weaknesses of Cell Synchronization Protocols Based on Inhibition of DNA Synthesis.International journal of molecular sciences · 2021Review
- Joint changes in RNA, RNA polymerase II, and promoter activity through the cell cycle identify non-coding RNAs involved in proliferation.Scientific reports · 2021Article
- Release from cell cycle arrest with Cdk4/6 inhibitors generates highly synchronized cell cycle progression in human cell culture.Open biology · 2020Article
- Inhibition of the ATR-CHK1 Pathway in Ewing Sarcoma Cells Causes DNA Damage and Apoptosis via the CDK2-Mediated Degradation of RRM2.Molecular cancer research : MCR · 2020Article
- Pds5A and Pds5B Display Non-redundant Functions in Mitosis and Their Loss Triggers Chk1 Activation.Frontiers in cell and developmental biology · 2020Article
- Mapping Metabolic Events in the Cancer Cell Cycle Reveals Arginine Catabolism in the Committed SGCell reports · 2019Article
- DNA Replication Determines Timing of Mitosis by Restricting CDK1 and PLK1 Activation.Molecular cell · 2018Article
- Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage.Journal of visualized experiments : JoVE · 2018Article
- mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells.Molecular and cellular biology · 2017Article
- Review
- Cell cycle proliferation decisions: the impact of single cell analyses.The FEBS journal · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Several methods to synchronize cultured cells in the cell cycle are based on temporary inhibition of DNA replication. Previously it has been reported that cells synchronized this way exhibited significant growth imbalance and unscheduled expression of cyclins A and B1. We have now observed that HL-60 cells exposed to inhibitors of DNA replication (thymidine, aphidicolin and hydroxyurea), at concentrations commonly used to synchronize cell populations, had histone H2AX phosphorylated on Ser-139. This modification of H2AX, a marker of DNA damage (induction of DNA double-strand breaks; DSBs), was most pronounced in S-phase cells, and led to their apoptosis. Thus, to a large extent, synchronization was caused by selective kill of DNA replicating cells through induction of replication stress. In fact, similar synchronization has been achieved by exposure of cells to the DNA topoisomerase I inhibitor camptothecin, a cytotoxic drug known to target S-phase cells. A large proportion of the surviving cells 'synchronized' by DNA replication inhibitors at the G1/S boundary had phosphorylated histone H2AX. Inhibitors of DNA replication, thus, not only selectively kill DNA replicating cells, induce growth imbalance and alter the machinery regulating progression through the cycle, but they also cause DNA damage involving formation of DSBs in the surviving ('synchronized') cells. The above effects should be taken into account when interpreting data obtained with the use of cells synchronized by inhibitors of DNA replication.
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Registered trials
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