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1.
Methods Mol Biol ; 2511: 89-97, 2022.
Article in English | MEDLINE | ID: mdl-35838954

ABSTRACT

Since the outbreak of coronavirus disease 2019 (COVID-19) on the Diamond Princess cruise ship docked at Yokohama Port on February 3, 2020, real-time reverse transcription-polymerase chain reaction (RT-PCR) testing using nasopharyngeal swab samples from symptomatic and asymptomatic COVID-19 individuals has been the main way to detect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA in almost all clinical laboratories in Japan. With the diffusion of sets containing the primers and probe, the gold standard real-time RT-PCR test has permeated throughout the country. To prevent the spread of infection, real-time RT-PCR testing is important to confirm whether people are positive, asymptomatic, or negative for COVID-19. Now, in addition to pharyngeal swab, saliva and blood samples can be used to detect SARS-CoV-2 RNA. Here, we introduce a clinical laboratory test performed using the High Pure viral nucleic acid kit and subsequent real-time RT-PCR system to detect SARS-CoV-2 RNA in serum, plasma, or whole blood in a hospital in Yokohama, Japan.


Subject(s)
COVID-19 , SARS-CoV-2 , COVID-19/diagnosis , Clinical Laboratory Techniques , Humans , RNA, Viral/genetics , Reverse Transcriptase Polymerase Chain Reaction , SARS-CoV-2/genetics
2.
Adv Exp Med Biol ; 1327: 25-33, 2021.
Article in English | MEDLINE | ID: mdl-34279826

ABSTRACT

Since an outbreak of COVID-19 was detected among the crew and passengers of the Diamond Princess cruise ship in early 2020, the total number of cases of SARS-CoV-2 has surpassed 440,000 in Japan. However, that number remains small compared with other countries, such as the United States, a few European countries, and China. Despite the Japanese government not imposing a lockdown or implementing large-scale testing at the municipal level, the country has managed to contain the smaller outbreaks. To avoid infection, it is important to wear a face mask, wash one's hands, and observe social distancing. In addition, we focus on the clinical laboratory testing performed using the latest technology to detect SARS-CoV-2 RNA in a hospital in Yokohama, Japan. Large-scale testing of viral RNA would be useful for detecting asymptomatic virus carriers as is done in other countries, and could be carried out as a future measure for controlling COVID-19.


Subject(s)
COVID-19 , Quarantine , China , Communicable Disease Control , Disease Outbreaks/prevention & control , Europe , Humans , Japan/epidemiology , Prevalence , RNA, Viral , SARS-CoV-2 , Ships , United States
3.
Biochem Biophys Rep ; 23: 100796, 2020 Sep.
Article in English | MEDLINE | ID: mdl-32875124

ABSTRACT

Superoxide dismutases, which catalytically remove intracellular superoxide radicals by the disproportionation of molecular oxygen and hydrogen peroxide, are encoded by the sod-1 to -5 genes in the nematode C. elegans. Expression of the sod genes is mutually compensatory for the modulation of intracellular oxidative stress during aging. Interestingly, several-fold higher expression of the sod-1 to -4 was induced in a sod-5 deletion mutant, despite the low expression levels of sod-5 in wild-type animals. Consequently, this molecular compensation facilitated recovery of lifespan in the sod-5 mutant. In previous reports, two transcription factors DAF-16 and SKN-1 are associated with the compensatory expression of sod genes, which are downstream targets of the ins/IGF-1 and p38 MAPK signaling pathways activated under oxidative and heavy metal stresses, respectively. Here, we show that p38 MAPK signaling regulates induction of not only the direct expression of sod-1, -2 and -4 but also the indirect modulation of DAF-16 targets, such as sod-3 and -5 genes. Moreover, a SKN-1 target, the insulin peptide gene ins-5, partially mediates the expression of DAF-16 targets via p38 MAPK signaling. These findings suggest that the interaction of ins/IGF-1 and p38 MAPK signaling pathways plays an important role in the fine-tuning of molecular compensation among sod genes to protect against mitochondrial oxidative damage during aging.

4.
Methods Mol Biol ; 2138: 195-205, 2020.
Article in English | MEDLINE | ID: mdl-32219749

ABSTRACT

In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 (C. elegans p53-like protein) is associated not only with the stress response, germline apoptosis, and meiotic chromosome segregation but also with longevity through the modification of energy metabolism during aging. The mitochondrial respiration-related gene sco-1 in C. elegans is orthologous to the human SCO1 gene and a target of p53/CEP-1. Using quantitative real-time polymerase chain reaction (PCR) analysis, we recently found that the expression levels of sco-1 gene were increased in wild-type C. elegans in an aging-related manner and decreased in long-lived cep-1 mutants. Here, we describe the relative quantitative strategy using a commercial real-time PCR system to detect more accurately differences in the levels of expressed genes between long-lived and wild-type C. elegans strains. To estimate the expression levels of target genes compared with wild-type using relative quantification, we used the expression levels of an endogenous control gene, such as a housekeeping gene. In addition, it is critical to normalize differences in the expression levels of the common housekeeping gene among the strains analyzed for an accurate comparison of the quantitative expression levels of target genes.


Subject(s)
Caenorhabditis elegans/genetics , Energy Metabolism/genetics , Genes, Helminth/genetics , Longevity/genetics , Real-Time Polymerase Chain Reaction/methods , Animals , Apoptosis/genetics , Caenorhabditis elegans Proteins/genetics , Gene Expression Regulation/genetics , Germ Cells/physiology
5.
Adv Exp Med Biol ; 1134: 163-175, 2019.
Article in English | MEDLINE | ID: mdl-30919337

ABSTRACT

Changes in energy metabolism occur not only in diseases such as cancer but also in the normal development and aging processes of various organisms. These metabolic changes result to lead to imbalances in energy metabolism related to cellular and tissue homeostasis. In the model organism C. elegans, which is used to study aging, an imbalance in age-related energy metabolism exists between mitochondrial oxidative phosphorylation and aerobic glycolysis. Cellular lactate and pyruvate are key intermediates in intracellular energy metabolic pathways and can indicate age-related imbalances in energy metabolism. Thus, the cellular lactate/pyruvate ratio can be monitored as a biomarker during aging. Moreover, recent studies have proposed a candidate novel biomarker for aging and age-related declines in the nematode C. elegans.


Subject(s)
Aging , Caenorhabditis elegans/metabolism , Energy Metabolism , Mitochondria/metabolism , Animals , Caenorhabditis elegans/physiology , Lactic Acid , Oxidative Phosphorylation , Pyruvic Acid
6.
Methods Mol Biol ; 1916: 123-132, 2019.
Article in English | MEDLINE | ID: mdl-30535690

ABSTRACT

In the nematode Caenorhabditis elegans (C. elegans), monitoring the lactate/pyruvate ratio in cells helps to detect imbalances in age-related energy metabolism. Here, we describe a modified small-scale extraction in C. elegans and measurement of lactate and pyruvate concentrations using colorimetric assay kits. During sample extraction, protein precipitation is the most critical step for precise determination of intracellular metabolites in C. elegans. Moreover, improved sensitivity and accuracy of colorimetric assay kits contributed to measurements of metabolites in samples derived from small-scale extraction. Using these protocols, we recently detected a metabolic alteration that occurs during aging by the monitoring the lactate/pyruvate ratio in a long-lived mutant of the mammalian tumor suppressor p53 ortholog CEP-1 in C. elegans.


Subject(s)
Caenorhabditis elegans Proteins/genetics , Colorimetry/methods , Lactic Acid/metabolism , Pyruvic Acid/metabolism , Tumor Suppressor Protein p53/genetics , Animals , Caenorhabditis elegans/metabolism , Caenorhabditis elegans Proteins/metabolism , Energy Metabolism/genetics , Humans , Longevity/genetics , Mutation/genetics
7.
J Vis Exp ; (140)2018 10 15.
Article in English | MEDLINE | ID: mdl-30371679

ABSTRACT

Lactate and pyruvate are key intermediates of intracellular energy metabolic pathways. Monitoring the lactate/pyruvate ratio in cells helps to determine whether there is an imbalance in age-related energy metabolism between mitochondrial oxidative phosphorylation and aerobic glycolysis. Here, we show the utilization of commercial colorimetric assay kits for lactate and pyruvate in the model organism C. elegans. Recently, the sensitivity and accuracy of the colorimetric/fluorimetric assay kits have been improved greatly by the research and development conducted by reagent manufacturers. The improved reagents have enabled the use of small-scale assays with a 96-well plate in C. elegans. In general, a fluorimetric assay is superior in sensitivity to a colorimetric assay; however, the colorimetric approach is more suitable for the use in common laboratories. Another important issue in these assays for quantitative determination is protein precipitation of homogenized C. elegans samples. In our protein precipitation method, common precipitants (e.g., trichloroacetic acid, perchloric acid and metaphosphoric acid) are used for sample preparation. A protein-free assay sample is prepared by directly adding cold precipitant (final concentration of 5%) during homogenization.


Subject(s)
Caenorhabditis elegans/metabolism , Colorimetry , Lactic Acid/analysis , Pyruvic Acid/analysis , Animals , Caenorhabditis elegans/chemistry , Lactic Acid/metabolism , Mitochondria/chemistry , Mitochondria/metabolism , Pyruvic Acid/metabolism
8.
Genes Cells ; 22(12): 1004-1010, 2017 Dec.
Article in English | MEDLINE | ID: mdl-29114996

ABSTRACT

In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 mediates the stress response, activates germ line apoptosis and regulates meiotic chromosome segregation. A reduction in its expression, which frequently occurs in mammalian cancer cells, extends lifespan and induces an adaptive response in C. elegans. However, these effects do not involve an increase in oxidative stress resistance. Here, we showed that intermittent exposure to hyperoxia, which induces oxidative stress resistance and lowers the production of ROS derived from mitochondrial respiration in C. elegans, slightly improved the lifespan extension of cep-1 mutant. Interestingly, ATP levels were increased without an increase in oxygen consumption in cep-1 mutant during aging. In the wild-type, lactate levels and consequentially the lactate/pyruvate ratio decreased during aging in adults. Furthermore, the expression levels of mitochondrial respiration-related sco-1, which is a target of p53/CEP-1, as well as those of gluconeogenesis regulation and mammalian sirtuin ortholog genes, were also increased in the aged and adaptive conditioned wild-type animals. In contrast, the lactate/pyruvate ratio increased in cells of the cep-1 mutant and was amplified by intermittent hyperoxia. These results suggest that impaired p53/CEP-1 leads to an imbalance in the age-related energy metabolic alteration between mitochondrial oxidative phosphorylation and aerobic glycolysis and plays an important role in the extension of both intact and adaptive lifespans.


Subject(s)
Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans/growth & development , Energy Metabolism , Longevity/physiology , Mitochondria/metabolism , Tumor Suppressor Protein p53/metabolism , Animals , Animals, Genetically Modified , Caenorhabditis elegans/genetics , Caenorhabditis elegans/metabolism , Caenorhabditis elegans Proteins/genetics , Lactic Acid/metabolism , Mutation , Oxygen Consumption , Pyruvic Acid/metabolism , Signal Transduction , Tumor Suppressor Protein p53/genetics
9.
Mech Ageing Dev ; 133(9-10): 600-10, 2012.
Article in English | MEDLINE | ID: mdl-22898738

ABSTRACT

The lifespans of many poikilothermic animals, including the nematode Caenorhabditis elegans, depend significantly on environmental temperature. Using long-living, thermosensory mutants of C. elegans, we tested whether the temperature dependency of the mean lifespan is compatible with the Arrhenius equation, which typically represents one of the chemical reaction rate theories. The temperature dependency of C. elegans was the Arrhenius type or normal, but daf-2(e1370) mutants were quite different from the others. However, taking into account the effect of the thermal denaturation of DAF-2 with the temperature, we showed that our analyzed results are compatible with previous ones. We investigated the timing mechanism of one parameter (the onset of biodemographic aging (t(0))) in the lifespan equation by applying the RNAi feeding method to daf-2 mutants in order to suppress daf-16 activity at different times during the life cycle. In summary, we further deepened the biological role of two elements, t(0) and z (the inverse of the aging rate), in the lifespan equation and mean lifespan formulated by our diffusion model z(2) = 4Dt(0), where z is composed of t(0) and D (the diffusion constant).


Subject(s)
Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans/metabolism , Hot Temperature , Longevity , Models, Biological , Mutation , Receptor, Insulin/metabolism , Animals , Caenorhabditis elegans/genetics , Caenorhabditis elegans Proteins/genetics , Protein Denaturation , Receptor, Insulin/genetics
10.
Oxid Med Cell Longev ; 2011: 596240, 2011.
Article in English | MEDLINE | ID: mdl-22013497

ABSTRACT

Astaxanthin (AX), which is produced by some marine animals, is a type of carotenoid that has antioxidative properties. In this study, we initially examined the effects of AX on the aging of a model organism C. elegans that has the conserved intracellular pathways related to mammalian longevity. The continuous treatments with AX (0.1 to 1 mM) from both the prereproductive and young adult stages extended the mean lifespans by about 16-30% in the wild-type and long-lived mutant age-1 of C. elegans. In contrast, the AX-dependent lifespan extension was not observed even in a daf-16 null mutant. Especially, the expression of genes encoding superoxide dismutases and catalases increased in two weeks after hatching, and the DAF-16 protein was translocated to the nucleus in the AX-exposed wild type. These results suggest that AX protects the cell organelle mitochondria and nucleus of the nematode, resulting in a lifespan extension via an Ins/IGF-1 signaling pathway during normal aging, at least in part.


Subject(s)
Antioxidants/pharmacology , Caenorhabditis elegans/drug effects , Longevity/drug effects , Signal Transduction/drug effects , Animals , Caenorhabditis elegans Proteins/analysis , Caenorhabditis elegans Proteins/genetics , Caenorhabditis elegans Proteins/metabolism , Catalase/metabolism , Cell Nucleus/metabolism , Forkhead Transcription Factors , Insulin/metabolism , Insulin-Like Growth Factor I/metabolism , Mutation , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Superoxide Dismutase/metabolism , Superoxides/metabolism , Transcription Factors/analysis , Transcription Factors/genetics , Transcription Factors/metabolism , Xanthophylls/pharmacology
11.
J Radiat Res ; 51(2): 107-21, 2010.
Article in English | MEDLINE | ID: mdl-20208402

ABSTRACT

The study of radiation effect in Caenorhabditis (C.) elegans has been carried out over three decades and now allow for understanding at the molecular, cellular and individual levels. This review describes the current knowledge of the biological effects of ionizing irradiation with a scope of the germ line, aging and behavior. In germ cells, ionizing radiation induces apoptosis, cell cycle arrest and DNA repair. Lots of molecules involved in these responses and functions have been identified in C. elegans, which are highly conserved throughout eukaryotes. Radiosensitivity and the effect of heavy-ion microbeam irradiation on germ cells with relationship between initiation of meiotic recombination and DNA lesions are discussed. In addition to DNA damage, ionizing radiation produces free radicals, and the free radical theory is the most popular aging theory. A first signal transduction pathway of aging has been discovered in C. elegans, and radiation-induced metabolic oxidative stress is recently noted for an inducible factor of hormetic response and genetic instability. The hormetic response in C. elegans exposed to oxidative stress is discussed with genetic pathways of aging. Moreover, C. elegans is well known as a model organism for behavior. The recent work reported the radiation effects via specific neurons on learning behavior, and radiation and hydrogen peroxide affect the locomotory rate similarly. These findings are discussed in relation to the evidence obtained with other organisms. Altogether, C. elegans may be a good "in vivo" model system in the field of radiation biology.


Subject(s)
Aging/radiation effects , Behavior, Animal/radiation effects , Caenorhabditis elegans/radiation effects , Germ Cells/radiation effects , Animals , Apoptosis/radiation effects , Caenorhabditis elegans/embryology , Caenorhabditis elegans/growth & development , Caenorhabditis elegans/physiology , DNA, Helminth/radiation effects , Disorders of Sex Development , Gametogenesis/radiation effects , Learning/radiation effects , Locomotion/radiation effects , Meiosis/radiation effects , Models, Animal , Oxidative Stress , Radiation Tolerance , Signal Transduction/radiation effects
12.
J Radiat Res ; 51(1): 67-71, 2010.
Article in English | MEDLINE | ID: mdl-19851044

ABSTRACT

The time spent as a dauer larva does not affect adult life span in Caenorhabditis elegans, as if aging is suspended in this quiescent developmental stage. We now report that modest doses X-irradiation of dauer larvae increased their post-dauer longevity. Post-irradiation incubation of young dauer larvae did not modify this beneficial effect of radiation. Conversely, holding dauer larvae prior to irradiation rendered them refractory to this X-radiation-induced response. We present a model to explain these results. These experiments demonstrate that dauer larvae provide an excellent opportunity to study mechanisms by which X irradiation can extend life span.


Subject(s)
Caenorhabditis elegans/physiology , Caenorhabditis elegans/radiation effects , Longevity/physiology , Longevity/radiation effects , Animals , Dose-Response Relationship, Radiation , Larva/physiology , Larva/radiation effects , Radiation Dosage
13.
J Gerontol A Biol Sci Med Sci ; 64(5): 530-9, 2009 May.
Article in English | MEDLINE | ID: mdl-19282511

ABSTRACT

Superoxide dismutase (SOD) is an enzyme that catalytically removes the superoxide radical (*O2-) and protects organisms from oxidative damage during normal aging. We demonstrate that not only the cytosolic *O2- level but also the mitochondrial *O2- level increases in the deletion mutants of sod-1 gene encoding Cu/Zn SOD in Caenorhabditis elegans (C. elegans). Interestingly, this suggests that the activity of SOD-1, which so far has been thought to act mainly in cytoplasm, helps to control the detoxification of *O2- also in the mitochondria. We also found functional compensation by other SODs, especially the sod-5 gene, which was induced several fold in the mutants. Therefore, the possibility exists that the compensative expression of sod-5 gene in the sod-1 deficit is associated with the insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, which regulates longevity and stress resistance of C. elegans because the sod-5 gene may be a target of the pathway.


Subject(s)
Gene Expression Regulation, Enzymologic , Longevity/genetics , Mitochondria/enzymology , Reactive Oxygen Species/metabolism , Superoxide Dismutase/genetics , Animals , Caenorhabditis elegans , Superoxide Dismutase-1
14.
J Radiat Res ; 50(2): 119-25, 2009 Mar.
Article in English | MEDLINE | ID: mdl-19194068

ABSTRACT

Locomotory behavior (motility) and mechanosensation are of vital importance in animals. We examined the effects of ionizing radiation (IR) on locomotory behavior and mechanosensation using a model organism, the nematode Caenorhabditis elegans. Bacterial mechanosensation in C. elegans induces the dopamine-mediated slowing of locomotion in the presence of bacteria (food), known as the basal slowing response. We previously reported an IR-induced reduction of locomotory rate in the absence of food. In the present study, we observed a similar IR-induced reduction of locomotory rate in the cat-2 mutant, which is defective in bacterial mechanosensation. The dose response pattern of the locomotory rate in the presence of food was relatively flat in wild-type animals, but not in cat-2 mutants. This suggests that the dopamine system, which is related to bacterial mechanosensation in C. elegans, might have a dominant effect on locomotory rate in the presence of food, which masks the effects of other stimuli. Moreover, we found that the behavioral responses of hydrogen peroxide-exposed wild-type animals are similar to those of IR-exposed animals. Our findings suggest that the IR-induced reduction of locomotory rate in the absence of food is mediated by a different pathway from that for bacterial mechanosensation, at least partially through IR-produced hydrogen peroxide.


Subject(s)
Caenorhabditis elegans/radiation effects , Locomotion/radiation effects , Motor Activity/radiation effects , Radiation, Ionizing , Tyrosine 3-Monooxygenase/genetics , Animals , Behavior, Animal/radiation effects , Caenorhabditis elegans Proteins/genetics , Caenorhabditis elegans Proteins/physiology , Chemoreceptor Cells/metabolism , Dose-Response Relationship, Drug , Dose-Response Relationship, Radiation , Hydrogen Peroxide/metabolism , Hydrogen Peroxide/pharmacology , Models, Biological , Mutation , Oxidative Stress , Tyrosine 3-Monooxygenase/physiology
15.
J Radiat Res ; 49(3): 285-91, 2008 May.
Article in English | MEDLINE | ID: mdl-18296869

ABSTRACT

Learning impairment following ionizing radiation (IR) exposure is an important potential risk in manned space missions. We previously reported the modulatory effects of IR on salt chemotaxis learning in Caenorhabditis elegans. However, little is known about the effects of IR on the functional relationship in the nervous system. In the present study, we investigated the effects of gamma-ray exposure on the relationship between locomotion and salt chemotaxis learning behavior. We found that effects of pre-learning irradiation on locomotion were significantly correlated with the salt chemotaxis learning performance, whereas locomotion was not directly related to chemotaxis to NaCl. On the other hand, locomotion was positively correlated with salt chemotaxis of animals which were irradiated during learning, and the correlation disappeared with increasing doses. These results suggest an indirect relationship between locomotion and salt chemotaxis learning in C. elegans, and that IR inhibits the innate relationship between locomotion and chemotaxis, which is related to salt chemotaxis learning conditioning of C. elegans.


Subject(s)
Gamma Rays , Learning/radiation effects , Locomotion/radiation effects , Animals , Caenorhabditis elegans/radiation effects , Chemotaxis/radiation effects , Salts
16.
J Radiat Res ; 49(3): 211-8, 2008 May.
Article in English | MEDLINE | ID: mdl-18285659

ABSTRACT

The hormetic effect, which extends the lifespan by various stressors, has been confirmed in Caenorhabditis elegans (C. elegans). We have previously reported that oxidative stress resistance in a long-lived mutant age-1 is associated with the hormesis. In the age-1 allele, which activates an insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, the superoxide dismutase (SOD) and catalase activities increased during normal aging. We now demonstrate changes in the mitochondrial superoxide radical (*O(2)(-)) levels of the hormetic conditioned age-related strains. The *O(2)(-) levels in age-1 strain significantly decreased after intermittent hyperoxia exposure. On the other hand, this phenomenon was not observed in a daf-16 null mutant. This hormesis-dependent reduction of the *O(2)(-) levels was observed even if the mitochondrial Mn-SOD was experimentally reduced. Therefore, it is indicated that the hormesis is mediated by events that suppress the mitochondrial *O(2)(-) production. Moreover, some SOD gene expressions in the hormetic conditioned age-1 mutant were induced over steady state mRNA levels. These data suggest that oxidative stress-inducible hormesis is associated with a reduction of the mitochondrial *O(2)(-) production by activation of the antioxidant system via the Ins/IGF-1 signaling pathway.


Subject(s)
Caenorhabditis elegans Proteins/genetics , Insulin-Like Growth Factor I/physiology , Insulin/physiology , Mitochondria/chemistry , Phosphatidylinositol 3-Kinases/genetics , Signal Transduction/physiology , Superoxides/analysis , Animals , Caenorhabditis elegans/genetics , Caenorhabditis elegans/physiology , Longevity/physiology , Mutation
17.
FASEB J ; 22(3): 713-20, 2008 Mar.
Article in English | MEDLINE | ID: mdl-17947388

ABSTRACT

Ionizing radiation (IR) is known to impair learning by suppressing adult neurogenesis in the hippocampus. However, in a mature nervous system, IR-induced functional alterations that are independent of neurogenesis remain largely unknown. In the present study, we analyzed the effects of IR on a food-NaCl associative learning paradigm of adult Caenorhabditis elegans that does not undergo neurogenesis. We observed that a decrease in chemotaxis toward NaCl occurs only after combined starvation and exposure to NaCl. Exposure to IR induced an additional decrease in chemotaxis immediately after an acute dose in the transition stage of the food-NaCl associative learning. Strikingly, chronic irradiation induced negative chemotaxis in the exposed animals, i.e., the primary avoidance response. IR-induced additional decreases in chemotaxis after acute and chronic irradiation were significantly suppressed in the gpc-1 mutant, which was defective in GPC-1 (one of the two gamma subunits of the heterotrimeric G-protein). Chemotaxis to cAMP, but not to lysine and benzaldehyde, was influenced by IR during the food-NaCl associative learning. Our novel findings suggest that IR behaves as a modulator in the food-NaCl associative learning via C. elegans GPC-1 and a specific neuronal network and may shed light on the modulatory effect of IR on learning.


Subject(s)
Association Learning/radiation effects , Caenorhabditis elegans Proteins/physiology , Caenorhabditis elegans/physiology , Food , GTP-Binding Protein gamma Subunits/physiology , Gamma Rays , Sodium Chloride/pharmacology , Animals , Association Learning/drug effects , Association Learning/physiology , Benzaldehydes/pharmacology , Caenorhabditis elegans/drug effects , Caenorhabditis elegans/radiation effects , Caenorhabditis elegans Proteins/drug effects , Caenorhabditis elegans Proteins/genetics , Chemotaxis/drug effects , Chemotaxis/radiation effects , Conditioning, Classical/drug effects , Conditioning, Classical/physiology , Conditioning, Classical/radiation effects , Cyclic AMP/pharmacology , Dose-Response Relationship, Drug , GTP-Binding Protein gamma Subunits/drug effects , GTP-Binding Protein gamma Subunits/genetics , Lysine/pharmacology , Mutation
18.
Mech Ageing Dev ; 126(6-7): 637-41, 2005.
Article in English | MEDLINE | ID: mdl-15888316

ABSTRACT

Mutations in the mev-1 and gas-1 genes of the nematode Caenorhabditis elegans render animals hypersensitive to oxygen and paraquat, and lead to premature aging. We show that both mutants overproduce superoxide anion in isolated sub-mitochondrial particles, which probably explains their hypersensitivity to oxidative stress. The daf-16 gene encodes a fork-head transcription factor that is negatively regulated by an insulin-signaling pathway. In wild-type animals, the DAF-16 protein normally resides in the cytoplasm and only becomes translocated to nuclei upon activating stimuli such as oxidative stress. Conversely, DAF-16 resides constitutively in the nuclei of mev-1 and gas-1 mutants even under normal growth conditions. Supplementation of the antioxidant coenzyme Q(10) reversed this nuclear translocation of DAF-16. Since both gas-1 and mev-1 encode subunits of electron transport chain complexes, these data illustrate how mitochondrial perturbations can impact signal transduction pathways.


Subject(s)
Aging, Premature/metabolism , Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans/metabolism , Cell Nucleus/metabolism , Mutation , Oxidative Stress , Transcription Factors/metabolism , Active Transport, Cell Nucleus/genetics , Aging, Premature/genetics , Animals , Caenorhabditis elegans Proteins/genetics , Cell Nucleus/genetics , Forkhead Transcription Factors , NADH Dehydrogenase/genetics , NADH Dehydrogenase/metabolism , Oxidative Stress/genetics , Oxygen/metabolism
19.
Mech Ageing Dev ; 126(6-7): 642-7, 2005.
Article in English | MEDLINE | ID: mdl-15888317

ABSTRACT

Much attention has focused on the insulin-like signaling pathway in Caenorhabditis elegans because of its pivotal role in life-span determination and oxidative stress resistance. The daf-16 gene encodes a fork-head transcription factor that is negatively regulated by this insulin-signaling pathway. The DAF-16 protein is translocated to the nucleus when animals were subjected to oxidative stress in the form of paraquat. This oxidative stress-mediated translocation was blocked by mutation of the p38-related sek-1 (MAPKK) mutant and DAF-16 instead remained cytoplasmic. The fact that DAF-16 translocation by oxidative stress is epistatic to sek-1 suggests that oxidative stress mediates regulation of DAF-16 through activating the p38 signal transduction pathway upstream of daf-16 so as to mobilize DAF-16 to the nucleus and activate transcription.


Subject(s)
Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans/physiology , Cell Nucleus/metabolism , MAP Kinase Signaling System/physiology , Oxidative Stress/physiology , Transcription Factors/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Active Transport, Cell Nucleus/drug effects , Active Transport, Cell Nucleus/genetics , Active Transport, Cell Nucleus/physiology , Animals , Caenorhabditis elegans/genetics , Caenorhabditis elegans Proteins/genetics , Cell Nucleus/genetics , Forkhead Transcription Factors , Herbicides/pharmacology , MAP Kinase Kinase 4/genetics , MAP Kinase Kinase 4/metabolism , MAP Kinase Signaling System/drug effects , MAP Kinase Signaling System/genetics , Oxidative Stress/drug effects , Oxidative Stress/genetics , Paraquat/pharmacology , Transcription Factors/genetics
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