ArticlePLoS computational biology2014
Robustness of DNA repair through collective rate control.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- Experimental Framework for Assessing Mouse Retinal Regeneration Through Single-Cell RNA-Sequencing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- A broadly applicable method for quantifying cardiomyocyte cell division identifies proliferative events following myocardial infarction.Cell reports methods · 2024Article
- The effect of Fernblock® in preventing blue-light-induced oxidative stress and cellular damage in retinal pigment epithelial cells is associated with NRF2 induction.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024Article
- Unscheduled DNA Synthesis at Sites of Local UV-induced DNA Damage to Quantify Global Genome Nucleotide Excision Repair Activity in Human Cells.Bio-protocol · 2023Article
- Retinoblastoma protein regulates carcinogen susceptibility at heterochromatic cancer driver loci.Life science alliance · 2022Article
- A constitutively expressed fluorescent ubiquitination-based cell-cycle indicator (FUCCI) in axolotls for studying tissue regeneration.Development (Cambridge, England) · 2022Article
- A Quantitative Model Explains Single-Cell Dynamics of the Adaptive Response in Escherichia coli.Biophysical journal · 2019Article
- Review: Precision medicine and driver mutations: Computational methods, functional assays and conformational principles for interpreting cancer drivers.PLoS computational biology · 2019Review
- Carcinogen susceptibility is regulated by genome architecture and predicts cancer mutagenesis.The EMBO journal · 2017Article
- Quantitative Systems Biology to decipher design principles of a dynamic cell cycle network: the "Maximum Allowable mammalian Trade-Off-Weight" (MAmTOW).NPJ systems biology and applications · 2017Review
- Mechanistic Modelling and Bayesian Inference Elucidates the Variable Dynamics of Double-Strand Break Repair.PLoS computational biology · 2016Article
- Subnuclear localization, rates and effectiveness of UVC-induced unscheduled DNA synthesis visualized by fluorescence widefield, confocal and super-resolution microscopy.Cell cycle (Georgetown, Tex.) · 2016Article
- Cellular Recognition and Repair of Monofunctional-Intercalative Platinum--DNA Adducts.Chemical research in toxicology · 2015Article
- The structural basis for cancer treatment decisions.Oncotarget · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA repair and other chromatin-associated processes are carried out by enzymatic macromolecular complexes that assemble at specific sites on the chromatin fiber. How the rate of these molecular machineries is regulated by their constituent parts is poorly understood. Here we quantify nucleotide-excision DNA repair in mammalian cells and find that, despite the pathways' molecular complexity, repair effectively obeys slow first-order kinetics. Theoretical analysis and data-based modeling indicate that these kinetics are not due to a singular rate-limiting step. Rather, first-order kinetics emerge from the interplay of rapidly and reversibly assembling repair proteins, stochastically distributing DNA lesion repair over a broad time period. Based on this mechanism, the model predicts that the repair proteins collectively control the repair rate. Exploiting natural cell-to-cell variability, we corroborate this prediction for the lesion-recognition factor XPC and the downstream factor XPA. Our findings provide a rationale for the emergence of slow time scales in chromatin-associated processes from fast molecular steps and suggest that collective rate control might be a widespread mode of robust regulation in DNA repair and transcription.
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Registered trials
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.