Cited by 862Genetics, Aging, and Longevity in Model OrganismsPhysiological and biochemical adaptationsTardigrade Biology and Ecology

Thermotolerance and extended life-span conferred by single-gene mutations and induced by thermal stress

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Lithgow, G J, White, T M, Melov, S, Johnson, T E·1995·Proceedings of the National Academy of Sciences

Abstract

We have discovered that three longevity mutants of the nematode Caenorhabditis elegans also exhibit increased intrinsic thermotolerance (Itt) as young adults. Mutation of the age-1 gene causes not only 65% longer life expectancy but also Itt. The Itt phenotype cosegregates with age-1. Long-lived spe-26 and daf-2 mutants also exhibit Itt. We investigated the relationship between increased thermotolerance and increased life-span by developing conditions for environmental induction of thermotolerance. Such pretreatments at sublethal temperatures induce significant increases in thermotolerance and small but statistically highly significant increases in life expectancy, consistent with a causal connection between these two traits. Thus, when an animal's resistance to stress is increased, by either genetic or environmental manipulation, we also observe an increase in life expectancy. These results suggest that ability to respond to stress limits the life expectancy of C. elegans and might do so in other metazoa as well.

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Crossref · 10.1073/pnas.92.16.7540

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  • Increased chaperone induction leads to increased longevity both in uni- and multicellular organisms.

    “Numerous studies support now that increased chaperone induction leads to increased longevity both in uni- and multicellular organisms (Lithgow et al., 1995; Shama et al., 1998; Tatar et al., 1997).”

    From Protein Homeostasis and Aging: the importance of exquisite quality control (2011) · cites this paper as Lithgow et al., 1995

    The Results and Discussion report that mild thermal stress increased both thermotolerance and lifespan in C. elegans, a multicellular organism. But the Discussion treats lifespan extension through increased heat-shock-protein expression as a model and explicitly says that the causal prediction still needs testing. This paper does not establish the claimed effect of chaperone induction or report it in unicellular organisms. (LLM, conf=0.88)

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Research works printed but not linked: 8

  1. [7]Riddle, D. L. (1988) in The Nematode Caenorhabditis elegans, ed. Wood, W. B. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 393-412.
  2. [14]Larsen, P. L. (1993) Proc. Natl. Acad. Sci. USA 90, 8905–8909.
  3. [17]Fargnoli, J., Kunisada, T., Fornace, A. J., Schneider, E. L. & Holbrook, N. J. (1990) Proc. Natl. Acad. Sci. USA 87, 846–850.
  4. [19]Šulston, J. & Hodgkin, J. (1988) in The Nematode Caenorhabditis elegans, ed. Wood, W. B. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 589–606.
  5. [21]Lee, É. T. (1992) Statistical Methods for Survival Data Analysis (Wiley, New York).
  6. [23]Parsell, D. A. & Lindquist, S. (1994) in The Biology of Heat Shock Proteins and Molecular Chaperones, eds. Morimoto, R. I., Tissieres, A. & Georgopoulos, C. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 457–494.
  7. [34]Rose, M. R. (1991) Evolutionary Biology of Aging (Oxford Univ. Press, New York).
  8. [38]Morimoto, R. I., Tissieres, A. & Georgopoulos, C., eds. (1994) The Biology of Heat Shock Proteins and Molecular Chaperones (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 1–30.

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Authors
Lithgow, G. J., White, T. M., Melov, S., & Johnson, T. E.
Affiliations
Institute of Behavioral Genetics, Boulder, CO, USA.
Venue
Proceedings of the National Academy of Sciences
Published
1995-08
Volume
92
Issue
16
Pages
7540-7544
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2093935763
Cited by
862
References
1
Citations by year
2026: 14 · 2025: 16 · 2024: 24 · 2023: 25 · 2022: 25 · 2021: 20 · 2020: 22 · 2019: 27 · 2018: 30 · 2017: 26 · 2016: 34 · 2015: 33 · 2014: 37 · 2013: 35 · 2012: 38
FWCI
7.37
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5k02aa000195-07, 5r01ag008322-06, 5r01ag010248-03)
  • National Institute on Alcohol Abuse and Alcoholism (KO2 AA00195)
  • National Institute on Aging (R01 AG8322, R01AG10248)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Physical Sciences › Environmental Science › Ecology › Physiological and biochemical adaptations
  • Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Tardigrade Biology and Ecology
Keywords
heat tolerance, longevity, lifespan, Caenorhabditis elegans, daf-2, thermal stress (biology), stress tolerance, genetic mutations, life expectancy
MeSH terms
Aging, Alleles, Animals, Female, Hot Temperature, Longevity, Male, Mutation, Stress, Physiological, Caenorhabditis elegans, Genes, Helminth

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