Cited by 1,214Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceAutophagy in Disease and Therapy

Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans

Herndon, Laura A., Schmeissner, Peter J., Dudaronek, Justyna M., Brown, Paula A., Listner, Kristin M., Sakano, Yuko, Paupard, Marie C., Hall, David H. +1 more·2002·Nature

Abstract

The nematode Caenorhabditis elegans is an important model for studying the genetics of ageing, with over 50 life-extension mutations known so far. However, little is known about the pathobiology of ageing in this species, limiting attempts to connect genotype with senescent phenotype. Using ultrastructural analysis and visualization of specific cell types with green fluorescent protein, we examined cell integrity in different tissues as the animal ages. We report remarkable preservation of the nervous system, even in advanced old age, in contrast to a gradual, progressive deterioration of muscle, resembling human sarcopenia. The age-1(hx546) mutation, which extends lifespan by 60-100%, delayed some, but not all, cellular biomarkers of ageing. Strikingly, we found strong evidence that stochastic as well as genetic factors are significant in C. elegans ageing, with extensive variability both among same-age animals and between cells of the same type within individuals.

Integrity signals

Registry

Crossref · 10.1038/nature01135

Cites

52 of 52 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Ultrastructural studies in C. elegans showed vastly different rates of aging of tissues and cells in individual worms, ascribed largely to stochastic events, and the onset of degenerative changes was neither linear nor synchronized.

    “Ultrastructural studies in C. elegans almost two decades ago hinted that it might not.30 The authors noted not only vastly different rates of aging of tissues and cells in individual worms, which they ascribed largely to stochastic events, but the onset of degenerative changes was neither linear nor synchronized.”

    From Asynchronous, contagious and digital aging (2021) · cites this paper as [30]

  • In C. elegans, muscles undergo an aging-related ultrastructural deterioration (sarcopenia), whereas nervous system ultrastructure remains largely intact.

    “In the model organism C. elegans the muscles undergo an aging-related ultrastructural deterioration (also referred to as sarcopenia), whereas nervous system ultrastructure remains largely intact(Herndon et al., 2002).”

    From Programmed cell death in aging (2015) · cites this paper as Herndon et al., 2002

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Herndon, L. A., Schmeissner, P. J., Dudaronek, J. M., Brown, P. A., Listner, K. M., Sakano, Y., Paupard, M. C., Hall, D. H., & Driscoll, M.
Affiliations
  • Rutgers, The State University of New Jersey (US)
  • Albert Einstein College of Medicine (US)
Corresponding author
  • Hall, David H.
  • Driscoll, Monica
Venue
Nature
Published
2002-10
Volume
419
Issue
6909
Pages
808-814
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2034734284
Cited by
1,214
References
52
Citations by year
2026: 40 · 2025: 49 · 2024: 65 · 2023: 39 · 2022: 63 · 2021: 65 · 2020: 68 · 2019: 61 · 2018: 60 · 2017: 57 · 2016: 69 · 2015: 51 · 2014: 54 · 2013: 77 · 2012: 48
FWCI
9.31
Type
journal article
Language
en
Open access
closed
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
  • National Institutes of Health (R24OD010943)
  • National Center for Research Resources (R24RR012596)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Caenorhabditis elegans, aging, lifespan extension, sarcopenia, muscle degeneration, ultrastructure, interindividual variability, cell-to-cell variability
MeSH terms
Aging, Animals, Gene Expression Regulation, Humans, Locomotion, Longevity, Muscles, Mutation, Nervous System Physiological Phenomena, Neurons, Organ Specificity, Phenotype, Reproduction, Stochastic Processes, Time Factors, Biomarkers, Cellular Senescence, Caenorhabditis elegans, Genes, Helminth, Phosphatidylinositol 3-Kinases, Caenorhabditis elegans Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review