The DNA damage checkpoint response to replication stress: A Game of Forks
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Summary
How cells achieve checkpoint signaling inactivation once replication stress is overcome is discussed and how a failure to timely revert checkpoint-mediated changes in cellular physiology might impact on replication dynamics and genome integrity is discussed.
- Type
- article
- Published
- 2013-02-11
- Cited by
- 76
- References
- 161
- Access
- Open access
- OpenAlex
- https://openalex.org/W1984528393
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21079920
Keywords
G2-M DNA damage checkpoint, DNA re-replication, Genome instability, DNA replication, Cell cycle checkpoint
References
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- DNA replication checkpoint prevents precocious chromosome segregation by regulating spindle behavior.
- Cell-cycle checkpoints and cancer
- A single S phase double-strand break influences replicon dynamics and triggers a Mre11-Tel1/ATM-mediated mechanism controlling terminal fork integrity
- DNA damage signalling guards against activated oncogenes and tumour progression
- Uninterrupted MCM2-7 function required for DNA replication fork progression.
- Genome-organizing factors Top2 and Hmo1 prevent chromosome fragility at sites of S phase transcription.
- Control of ribonucleotide reductase localization through an anchoring mechanism involving Wtm1.
- The Role of Single-stranded DNA and Polymerase α in Establishing the ATR, Hus1 DNA Replication Checkpoint*
- Yeast DNA Damage-inducible Rnr3 Has a Very Low Catalytic Activity Strongly Stimulated after the Formation of a Cross-talking Rnr1/Rnr3 Complex*
- The DNA replication and damage checkpoint pathways induce transcription by inhibition of the Crt1 repressor.
- GINS maintains association of Cdc45 with MCM in replisome progression complexes at eukaryotic DNA replication forks
- ATR Homolog Mec1 Promotes Fork Progression, Thus Averting Breaks in Replication Slow Zones
Cited by
- Replisome‐Cohesin Interfacing: A Molecular Perspective
- Regulation of genome stability via Mcm2-7 ATPase active sites in Saccharomyces cerevisiae
- Regulation of Elg1 activity by phosphorylation
- Ionizing Radiation-Induced DNA Damage, Response, and Repair
- Human CST abundance determines recovery from diverse forms of DNA damage and replication stress
- ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
- Commentary: critical questions, misconceptions and a road map for improving the use of the lymphocyte cytokinesis-block micronucleus assay for in vivo biomonitoring of human exposure to genotoxic chemicals-a HUMN project perspective.
- Replisome Function During Replicative Stress Is Modulated by Histone H3 Lysine 56 Acetylation Through Ctf4
- Homologous recombination maintenance of genome integrity during DNA damage tolerance
- The amino-terminal tails of histones H2A and H3 coordinate efficient base excision repair, DNA damage signaling and postreplication repair in Saccharomyces cerevisiae
- Checkpoint-dependent RNR induction promotes fork restart after replicative stress
- Molecular mechanisms involved in initiation of the DNA damage response
- Functions of Fun30 Chromatin Remodeler in Regulating Cellular Resistance to Genotoxic Stress
- The replicometer is broken: telomeres activate cellular senescence in response to genotoxic stresses
- Xbp1 Directs Global Repression of Budding Yeast Transcription during the Transition to Quiescence and Is Important for the Longevity and Reversibility of the Quiescent State
- Early Telomerase Inactivation Accelerates Aging Independently of Telomere Length
- Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells
- Bacterial Proliferation: Keep Dividing and Don't Mind the Gap
- Checkpoint Regulation of Replication Forks: Global or Local?
- Targeting the replisome with transduced monoclonal antibodies triggers lethal DNA replication stress in cancer cells.
Related papers
- The G2-phase DNA-damage checkpoint.
- Geminin deploys multiple mechanisms to regulate Cdt1 before cell division thus ensuring the proper execution of DNA replication
- Cell-cycle checkpoint kinases: checking in on the cell cycle.
- Redundant control of rereplication in fission yeast
- Phosphoregulation of Cdt1 in G2 and M phases prevents re-replication independently of Geminin
- Expression of Cdc18/Cdc6 and Cdt1 during G2 phase induces initiation of DNA replication
- Phosphorylation of Minichromosome Maintenance 3 (MCM3) by Checkpoint Kinase 1 (Chk1) Negatively Regulates DNA Replication and Checkpoint Activation*
- Activation of the DNA damage checkpoint in mutants defective in DNA replication initiation.
- S-phase checkpoint proteins Tof1 and Mrc1 form a stable replication-pausing complex