ArticlePLoS biology2016
Interpreting the Dependence of Mutation Rates on Age and Time.
Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research progress on the role and mechanism of DNA damage repair in germ cell development.Frontiers in endocrinology · 2023Pooled it
- Article
- The Effect of Age and Sex on the Rate of Germline Mutations in Barn Owls.Genome biology and evolution · 2026Article
- Developmental speed and chronological time exert opposing effects on the spontaneous mutation rate inEvolution letters · 2026Article
- Evolution of the rate, molecular spectrum, and fitness effects of mutation under minimal selection in Caenorhabditis elegans.Genetics · 2026Article
- Spontaneous mutation rate and spectrum are modulated by organismal fitness.Science advances · 2026Article
- Controlling for life-history traits in vertebrates reveals that effective population size does not affect mutation rate or genome size.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Evolution of the rate, molecular spectrum, and fitness effects of mutation under minimal selection inbioRxiv : the preprint server for biology · 2026Article
- Towards an evolutionary baseline model ofbioRxiv : the preprint server for biology · 2025Article
- Prevalence and genetics of "de novo" MEN2 syndromes.The Journal of clinical endocrinology and metabolism · 2025Article
- Sex differences in transcription-associated mutagenesis in the human germline.bioRxiv : the preprint server for biology · 2025Article
- Relationship of Ageing to Insulin Resistance and Atherosclerosis.Metabolites · 2025Review
- Collateral mutagenesis funnels multiple sources of DNA damage into a ubiquitous mutational signature.bioRxiv : the preprint server for biology · 2025Article
- Estimates of the Mutation Rate per Year Can Explain Why the Molecular Clock Depends on Generation Time.Molecular biology and evolution · 2025Article
- Characterizing the Rates and Patterns of De Novo Germline Mutations in the Aye-Aye (Daubentonia madagascariensis).Molecular biology and evolution · 2025Article
- Quantifying cell divisions along evolutionary lineages in cancer.Nature genetics · 2025Article
- Experimental evolution and hybridization enhance the fermentative capacity of wild Saccharomyces eubayanus strains.FEMS yeast research · 2025Article
- On correlative and causal links of replicative epimutations.Trends in genetics : TIG · 2025Review
- Somatic mutation in autosomal dominant polycystic kidney disease revealed by deep sequencing human kidney cysts.NPJ genomic medicine · 2024Article
- Characterizing the rates and patterns ofbioRxiv : the preprint server for biology · 2024Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations can originate from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that arise between replication cycles and are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell divisions, providing a framework for understanding how mutation rates depend on sex, age, and cell division rate. We show that the accrual of mutations should track cell divisions not only when mutations are replicative in origin but also when they are non-replicative and repaired efficiently. One implication is that observations from diverse fields that to date have been interpreted as pointing to a replicative origin of most mutations could instead reflect the accumulation of mutations arising from endogenous reactions or exogenous mutagens. We further find that only mutations that arise from inefficiently repaired lesions will accrue according to absolute time; thus, unless life history traits co-vary, the phylogenetic "molecular clock" should not be expected to run steadily across species.
Indexed as
Identifiers
What OpenQuestion holds
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.