The longevity of<i>Caenorhabditis elegans</i>in soil

Voorhies, Wayne A. Van; Fuchs, Joseph R.; Thomas, Stephen

doi:10.1098/rsbl.2004.0278

Cited by 110 publications

(77 citation statements)

References 19 publications

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“…This is further supported by the finding that the loss of proteostasis in early adulthood corresponds to the same period during adult aging when polyglutamine-expansion proteins exhibit age-dependent aggregation and toxicity in C. elegans (20). It is interesting to note that the lifespan for WT C. elegans under laboratory conditions is 2-3 weeks, whereas in soil conditions this was reduced by nearly an order of magnitude (42). This would suggest that the maintenance of proteostasis is essential throughout development and extends only through the reproductive phase of adulthood, when there is an evolutionary advantage to allocate resources to proteostasis maintenance (41).…”

Section: Discussionsupporting

confidence: 60%

Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging

Ben‐Zvi

Miller

Morimoto

2009

Proc. Natl. Acad. Sci. U.S.A.

616

604

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Protein damage contributes prominently to cellular aging. To address whether this occurs at a specific period during aging or accumulates gradually, we monitored the biochemical, cellular, and physiological properties of folding sensors expressed in different tissues of C. elegans. We observed the age-dependent misfolding and loss of function of diverse proteins harboring temperature-sensitive missense mutations in all somatic tissues at the permissive condition. This widespread failure in proteostasis occurs rapidly at an early stage of adulthood, and coincides with a severely reduced activation of the cytoprotective heat shock response and the unfolded protein response. Enhancing stress responsive factors HSF-1 or DAF-16 suppresses misfolding of these metastable folding sensors and restores the ability of the cell to maintain a functional proteome. This suggests that a compromise in the regulation of proteostatic stress responses occurs early in adulthood and tips the balance between the load of damaged proteins and the proteostasis machinery. We propose that the collapse of proteostasis represents an early molecular event of aging that amplifies protein damage in age-associated diseases of protein conformation.daf-16 ͉ folding sensors ͉ hsf-1 ͉ protein misfolding ͉ stress response T he stability of the proteome is challenged by conditions that cause proteotoxic stress including errors during protein synthesis, oxidant-induced covalent modifications, inherited polymorphisms, and misfolding (1-3). Consequently, all cells have highly conserved stress-inducible pathways that detect, prevent, and resolve such damage (4, 5). Accumulation of misfolded proteins titrate the negative regulation of chaperones from HSF-1 (4, 6, 7). Likewise, an E3 ubiquitin ligase was shown to regulate the levels of DAF-16, also indicating a link between stress response activation to the balance between proteostasis capacity and the load of damaged proteins (8). The activation of cellular stress responses limits the accumulation of damaged proteins by suppression of misfolding and enhancing chaperonemediated folding, promoting the enzymatic removal of covalent modifications, and stimulating clearance by ubiquitin-mediated, proteosomal, and autophagic processes (1, 4, 5, 9, 10). The dynamics of these processes during aging, however, are poorly understood.Aging can be characterized by the loss of cellular function and increased vulnerability to environmental and physiological stress that results in enhanced susceptibility to disease. Many agedependent changes have been detected at mid-to-late lifespan of C. elegans, including the accumulation of damaged macromolecules, cell and organellar degeneration, and physiological decline (11-17). Likewise, aggregation and toxicity of diseaseassociated aggregation-prone proteins, such as huntingtin and A␤ peptide, is enhanced during aging in C. elegans and other model systems (18-21).The regulation of aging and the maintenance of proteostasis has been recently established in C. elegans. Downregulatio...

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Section: Discussionsupporting

confidence: 60%

Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging

Ben‐Zvi

Miller

Morimoto

2009

Proc. Natl. Acad. Sci. U.S.A.

616

604

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“…There exist many genetically characterized longevity mutants of C. elegans, and their study is an important and growing part of gerontology (10)(11)(12). There has been a huge amount of work undertaken on longevity genes relative to longevity extension and other traits including aspects of reproduction, competitive ability, and survival relative to environment and stresses (3,4,9,10,(13)(14)(15)(16)(17)(18).…”

mentioning

confidence: 99%

A Demographic Analysis of the Fitness Cost of Extended Longevity in Caenorhabditis elegans

Chen¹,

Şentürk²,

Wang³

et al. 2007

The Journals of Gerontology Series A: Biological Sciences and M

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We monitored survival and reproduction of 1000 individuals of Caenorhabditis elegans wild type (N2) and 800 individuals of clk-1 and daf-2, and used biodemographic analysis to address fitness as the integrative consequence of the entire age-specific schedules of survival and reproduction. Relative to N2, the mutants clk-1 and daf-2 extended average life span by 27% and 111%, respectively, but reduced net reproductive rate by 44% and 18%. The net result of differences in survival and fertility was a significant differential in fitness, with both clk-1 (k ¼ 2.74) and daf-2 (k ¼ 3.78) at a disadvantage relative to N2 (k ¼ 3.85). Demographic life table response experiment (LTRE) analysis revealed that the fitness differentials were due to negative effects in mutants on reproduction in the first 6-7 days of life. Fitness costs in clk-1 and daf-2 of C. elegans are consistent with the theory of antagonistic pleiotropy for the evolution of senescence.

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“…24) Under more natural conditions, the longevity of the daf-2 mutant, which exhibits 2-fold longer longevity than wild-type C. elegans under conventional laboratory conditions, was shorter than that of the wild-type worms. 24) S medium exhibits an extremely high osmolality, of 360 mOsm/kg, compared to those of Water media, of 14-25 mOsm/kg ( Table 2). The osmolalities of tap water and 2 mM NaOH solution, which showed similar conductivities, were 4 mOsm/kg.…”

Section: Discussionmentioning

confidence: 99%

Extension of the Lifespan ofCaenorhabditis elegansby the Use of Electrolyzed Reduced Water

Yan

Tian

Kinjo

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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The longevity ofCaenorhabditis elegansin soil

Cited by 110 publications

References 19 publications

Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging

Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging

A Demographic Analysis of the Fitness Cost of Extended Longevity in Caenorhabditis elegans

Extension of the Lifespan ofCaenorhabditis elegansby the Use of Electrolyzed Reduced Water

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