ArticleGenome research2002
Genome dynamics in aging mice.
Article in Genome research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed.
- The Impact of Environmental and Endogenous Damage on Somatic Mutation Load in Human Skin Fibroblasts.PLoS genetics · 2016Trial
- Review
- Aging at Evolutionary Crossroads: Longitudinal Gene Co-expression Network Analyses of Proximal and Ultimate Causes of Aging in Bats.Molecular biology and evolution · 2022Article
- From DNA damage to mutations: All roads lead to aging.Ageing research reviews · 2021Review
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging.Annual review of genetics · 2018Review
- Somatic mutation load and spectra: A record of DNA damage and repair in healthy human cells.Environmental and molecular mutagenesis · 2018Review
- Regulation of Drosophila Lifespan by bellwether Promoter Alleles.Scientific reports · 2017Article
- Do DNA Double-Strand Breaks Drive Aging?Molecular cell · 2016Review
- Unrevealed mosaicism in the next-generation sequencing era.Molecular genetics and genomics : MGG · 2016Review
- Using measures of single-cell physiology and physiological state to understand organismic aging.Aging cell · 2016Review
- Age-related somatic mutations in the cancer genome.Oncotarget · 2015Article
- NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1.Nature structural & molecular biology · 2015Article
- Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis.Genome research · 2014Article
- Resistance to genotoxic stresses in Arctica islandica, the longest living noncolonial animal: is extreme longevity associated with a multistress resistance phenotype?The journals of gerontology. Series A, Biological sciences and medical sciences · 2013Article
- Article
- Direct mutation analysis by high-throughput sequencing: from germline to low-abundant, somatic variants.Mutation research · 2012Review
- Measuring genome instability in aging - a mini-review.Gerontology · 2012Review
- Loss of the bloom syndrome helicase increases DNA ligase 4-independent genome rearrangements and tumorigenesis in aging Drosophila.Genome biology · 2011Article
- Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression.Oncogene · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Random spontaneous genome rearrangements are difficult to detect in vivo, especially in postmitotic tissues. Using a lacZ-plasmid reporter mouse model, we have previously presented evidence for the accumulation of large genome rearrangements in various tissues, including postmitotic tissues, during aging. These rearrangements, which were found to be organ-specific and to increase with age, have one breakpoint in the lacZ-reporter locus and the second elsewhere in the mouse genome. In this present work, we have used a mouse genome sequence database to physically characterize a total of 49 genome rearrangements in the brain, heart, and liver from young and old mice at two lacZ-plasmid reporter loci. Half of all breakpoints in the mouse genome occurred in chromosomes 3 and 4, each carrying a lacZ-reporter cluster, at distances varying from <100 kb to 66 Mb, indicating intrachromosomal deletions or inversions. The other half of the breakpoints in the mouse genome was found randomly on any of the other chromosomes, indicating translocations. Alternatively, part of the intra- and extrachromosomal events could involve transpositions. Regions of extended homology were not found at the breakpoints. These results lead us to postulate potential mechanisms for the origin of large genome rearrangements in mouse tissues and to predict their possible impact as a potential cause of aging.
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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.