Alterations of life span in the nematode Caenorhabditis elegans under monoxenic culture conditions

Hosono, Ryuji; Nishimoto, Sueo; Kuno, Sigeru

doi:10.1016/0531-5565(89)90016-8

Cited by 76 publications

(50 citation statements)

References 14 publications

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“…This process, called caloric restriction in many other species (Heininger 2002), is known in yeast (Lin et al 2000), nematodes (Hosono et al 1989), rodents (Weindruch and Walford 1988;Masoro 1998) and in primates and humans (Wanagat and Weindruch 2000). At the cellular level, caloric restriction inhibits the aging-related increase of mitochondrial ROS release and level of oxidative stress, and attenuates the decrease of antioxidant defences (Rao et al 1990;Gabitta et al 1997;Risby et al 1999, etc.).…”

Section: Implications For Future Research Strategymentioning

confidence: 99%

Review and perspectives of physiological mechanisms underlying genetically-based resistance of the Pacific oysterCrassostrea gigasto summer mortality

Samain

2011

Aquat. Living Resour.

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-French oyster farming has been subject to severe mortalities during the summer months. Results from the research program "Morest", which ran from 2000 to 2006 and examined the possible causes of these mortalities, led to the construction of a model to explain the interaction between environmental factors, oyster physiology and different opportunistic pathogens underlying oyster summer mortality. Temperature, food, reproduction and stress were the main factors required for oyster mortality. Genetically-based resistance ("R" oysters) or susceptibility ("S" oysters) to summer mortality was revealed by divergent selection. Building on these results, a literature search was made in 2007 on the molecular origin of genetic resistance to such a complex mortality risk. The objectives were to lay a foundation for the preparation and orientation of future research directions and to improve understanding of the underlying physiological mechanism leading to summer mortality. Three years later, the resulting conceptual analysis reported here was presented as an introductory lecture to Physiomar 2010, a conference where many new results contributing to this research field were also reported. The literature review highlighted two major review articles: the first dealing with nutrition and reproduction (Schneider 2004), the second with reproduction, temperature, oxidative stress and mortality (Heineinger 2002). The effect of nutrition level on energy orientation to growth or reproduction is controlled by endocrine factors. Among these, neuropeptide Y (NPY), ghrelin and leptin neuropeptides appeared to be potential candidates involved in germ-soma orientation in relation to trophic conditions. Depending on reproductive effort and temperature, a metabolic stress resulting from the germ-soma conflict can appear, characterized by mitochondrial reactive oxygen species (ROS) production. Such an excess of ROS induces perturbations in mitochondrial activity leading to cell death. Many organisms, such as annual plants or the Pacific salmon, do not survive their first reproduction. In contrast, others increase stress resistance by selection of antioxidant processes (superoxide dismutase SOD, catalase, etc.) through evolution, and survive first reproduction. A similar difference was observed in the comparison made between R and S oysters, which differed in ROS production, SOD and catalase levels. Such factors controlling reproduction and ROS detoxification processes could therefore provide new markers for selection of oysters with better resistance to non-specific pathogens, complementing other classic selection approaches against specific pathogens or for improved immunity. This antioxidant defence mechanism is found in many organisms including vertebrates and in some invertebrates, including oysters. Its role needs to be considered in pathology events involving other aquaculture species and it may also contribute to explaining the increase in marine pathologies under anthropogenic environmental changes.

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Section: Implications For Future Research Strategymentioning

confidence: 99%

Review and perspectives of physiological mechanisms underlying genetically-based resistance of the Pacific oysterCrassostrea gigasto summer mortality

Samain

2011

Aquat. Living Resour.

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“…The optical density (OD) of overnight-grown OP50 that had been washed with M9 buffer was taken as an index of food amount. Nematode growth medium assay plates were constituted without peptone to prevent additional growth of OP50 (Hosono et al, 1989). As shown in Fig.…”

Section: Metabolites Of Op50 Influence C Elegans Agingmentioning

confidence: 99%

GPA‐9 is a novel regulator of innate immunity against Escherichia coli foods in adult Caenorhabditis elegans

2011

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SummaryInnate immune responses to pathogens are governed by the nervous system. Here, we investigated the molecular mechanism underlying innate immunity in Caenorhabditis elegans against Escherichia coli OP50, a standard laboratory C. elegans food. Longevity was compared in worms fed live or UV-killed OP50 at low or high density food condition (HDF). Expression of the antimicrobial gene lys-8 was approximately 5-fold higher in worms fed live OP50, suggesting activation of innate immunity upon recognition of OP50 metabolites. Lifespan was extended and SOD-3 mRNA levels were increased in gpa-9-overexpressing gpa-9XS worms under HDF in association with robust induction of insulin ⁄ IGF-1 signaling (IIS). Expression of ins-7 and daf-28 that control lys-8 expression was reduced in gpa-9XS, indicating that GPA-9-mediated immunity is due in part to ins-7 and daf-28 downregulation. Our results suggest that OP50 metabolites in amphid neurons elicit innate immunity through the IIS pathway, and identify GPA-9 as a novel regulator of both the immune system and aging in C. elegans.

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“…Lowering food intake also lengthens C. elegans life span, indicating that the mechanism of CR may exist in the worm (32,33). We wondered whether any of the known genetic factors extending life span involve the same mechanism as food restriction.…”

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The genetics of caloric restriction in Caenorhabditis elegans

Lakowski

Hekimi

1998

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

881

749

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Low caloric intake (caloric restriction) can lengthen the life span of a wide range of animals and possibly even of humans. To understand better how caloric restriction lengthens life span, we used genetic methods and criteria to investigate its mechanism of action in the nematode Caenorhabditis elegans. Mutations in many genes (eat genes) result in partial starvation of the worm by disrupting the function of the pharynx, the feeding organ. We found that most eat mutations significantly lengthen life span (by up to 50%). In C. elegans, mutations in a number of other genes that can extend life span have been found. Two genetically distinct mechanisms of life span extension are known: a mechanism involving genes that regulate dauer formation (age-1, daf-2, daf-16, and daf-28) and a mechanism involving genes that affect the rate of development and behavior (clk-1, clk-2, clk-3, and gro-1). We find that the long life of eat-2 mutants does not require the activity of DAF-16 and that eat-2; daf-2 double mutants live even longer than extremely long-lived daf-2 mutants. These findings demonstrate that food restriction lengthens life span by a mechanism distinct from that of dauer-formation mutants. In contrast, we find that food restriction does not further increase the life span of long-lived clk-1 mutants, suggesting that clk-1 and caloric restriction affect similar processes.It was shown more than 50 years ago that reducing the caloric intake (caloric restriction) of rodents can significantly lengthen their mean and maximal life span (1). It subsequently has been shown that caloric restriction (CR) can lengthen the life span of a wide variety of animals (2). Trials have even begun with higher primates; based on preliminary evidence, calorically restricted rhesus monkeys show similar signs of delayed aging to those seen in the calorically restricted rodents (3-7). CR has been best studied in rodents, and it is known that rodents undergoing CR display many physiological changes, including reduced body weight, temperature, blood glucose, and insulin levels (reviewed in refs. 8 and 9). However, it is unclear which of these changes are required for an extended life span (8, 9). Several studies indicate that reducing caloric intake reduces the amount of damage attributable to free radicals (reviewed in refs. 8 and 9). One simple hypothesis to explain how CR extends life span is that CR may reduce basal metabolic rates. Rodents and primates undergoing CR have lowered body temperatures (10-12), an indication of lower metabolic rates. However, studies on the effect of CR on the metabolic rates of various mammals have given equivocal results, with some studies showing no change in oxygen consumption per unit of lean body mass (13,14) and other studies showing a decrease of consumption under CR (15, 16). In spite of uncertainty about how CR affects life span, it remains the only experimental treatment that has been shown repeatedly to significantly prolong the life of vertebrates (8,9,17).On the other hand, it is in Cae...

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Alterations of life span in the nematode Caenorhabditis elegans under monoxenic culture conditions

Cited by 76 publications

References 14 publications

Review and perspectives of physiological mechanisms underlying genetically-based resistance of the Pacific oysterCrassostrea gigasto summer mortality

Review and perspectives of physiological mechanisms underlying genetically-based resistance of the Pacific oysterCrassostrea gigasto summer mortality

GPA‐9 is a novel regulator of innate immunity against Escherichia coli foods in adult Caenorhabditis elegans

The genetics of caloric restriction in Caenorhabditis elegans

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