Bacillus licheniformis isolated from Korean traditional food resources enhances the lifespan of Caenorhabditis elegans through serotonin signaling
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE63056 | GEO | 2015/11/05
SECONDARY ACCESSION(S): PRJNA266520
REPOSITORIES: GEO
Similar Datasets
Project description:The C. elegans lifespan in the presence of Bacillus licheniformis caused induction of a large number of genes associated with anti-aging activiy including beta-oxidation Inaddition, these results indicate the B. licheniformis enhances the lifespan of Caenorhabditis elegans through serotonin signaling Two-condition experiment, C. elegans with B. lichemiformis 141 or E. coli OP50 (conrol) for 24 h. For preparing the total RNA, C. elegans were exposed to 20 mg of bacterial lawn in NGN agar for 24 h.
2015-11-05 | E-GEOD-63056 | biostudies-arrayexpress
Project description:Representative MS data of tph-1, pah-1, pah-1;tph-1, cat-2, bas-1, glo-1 and cest-4 mutant strains along with wildtype C. elegans. MS data of serotonin and 13C-isotope-labeled N-acetyrlserotonin treated wildtype C. elegans. MS data of neurotransmitter derivatization of tph-1, pah-1, pah-1;tph-1 and wildtype C. elegans. MS/MS data of serotonin treated wildtype C. elegans.
2022-01-30 | MSV000088750 | GNPS
Project description:Background: Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation. Methods: Two tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips). Results: In both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion. Conclusions: Altered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.
2014-10-31 | GSE57189 | GEO
Project description:Background: Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation. Methods: Two tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips). Results: In both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion. Conclusions: Altered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.
2014-10-31 | GSE57188 | GEO
Project description:Complete Genome Sequence of Latilactobacillus sakei subsp. sakei strain BM5
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Project description:Environmental factors such as temperature can modulate animal’s lifespan. However, the underlying mechanisms remain largely undefined. Through proteomic analysis of C. elegans at different time points (young adult, middle age, and old age) and under two temperature conditions (20°C and 25°C), we found that temperature affects C. elegans lifespan largely by modulating the proteostasis. Surprisingly, although animals live shorter at the higher temperature, we found that worms cultured at 25°C for one day at early adulthood promotes the protein homeostasis by decreasing the synthesis and increasing the degradation, suggesting the beneficial effects. Consistent with the finding, animals shifting from 20°C to 25°C for 24 hours between the larval L4 to adult Day 3 stages indeed live longer and are more resistant to stresses. Furthermore, we found that the one-day thermal induced lifespan extension is mediated by the FOXO transcriptional factor DAF-16. These results reveal an unexpected and complicated mechanism underlying the temperature effects on aging, which could potentially aid to develop strategies for treating aging related diseases.
2023-03-11 | PXD024916 | Pride
Project description:Many studies have addressed the effect of dietary glycemic index on obesity and diabetes, but little is known about its effect on lifespan itself. We found that adding a small amount of glucose to the medium (0.1-2%) shortened the lifespan of C. elegans. Glucose shortened lifespan by inhibiting the activities of lifespan-extending transcription factors that are also inhibited by insulin signaling: the FOXO family member DAF-16 and the heat shock factor HSF-1. This effect involved the down-regulation of an aquaporin glycerol channel, aqp-1. We show that changes in glycerol metabolism are likely to underlie the lifespan-shortening effect of glucose, and that aqp-1 may act cell non-autonomously as a feedback regulator in the insulin/IGF-1 signaling pathway. Insulin down-regulates similar glycerol channels in mammals, suggesting that this glucose-responsive pathway might be conserved evolutionarily. Together these findings raise the possibility that a low-sugar diet might have beneficial effects on lifespan in higher organisms. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture
2010-05-16 | E-GEOD-18563 | biostudies-arrayexpress
Project description:In the present study, a new biocontrol strain, Bacillus subtilis KU-153, was isolated from the Korean traditional fermented food Kimchi and evaluated for its ability to reduce the ochratoxin A (OTA) content in culture medium. A 16?S rRNA gene sequencing analysis revealed the identity of newly isolated strain KU-153 as B. subtilis. The growth kinetic study of B. subtilis KU-153, in terms of the OTA reduction in culture medium, confirmed its biocontrol efficacy. To verify its ability to reduce the OTA content in culture medium, bacterial extracts (intracellular and extracellular) of B. subtilis were separated and compared with whole B. subtilis cells (viable and heat-killed). No reduction in the OTA content was observed in culture medium with extracellular and intracellular extracts, while viable and heat-killed cells of B. subtilis showed significant levels (p?<?0.05) of OTA reduction in culture medium. Interestingly, B. subtilis heat-treated cells showed a higher OTA reduction (45%) than viable cells (22%). Further, B. subtilis heat-treated cells were assessed for their ability to reduce OTA levels in artificially contaminated red wine samples that resulted in an OTA reduction of approximately 90%, suggesting the biocontrol potential of the newly isolated strain B. subtilis KU-153 on OTA reduction.
| S-EPMC5966461 | biostudies-literature
Project description:Vaccinia virus-related kinase (VRK) is an evolutionarily conserved nuclear protein kinase. VRK-1, the single Caenorhabditis elegans VRK ortholog, functions in cell division and germline proliferation. However, the role of VRK-1 in post-mitotic cells and adult lifespan remain unknown. Here, we show that VRK-1 increases organismal longevity by activating the cellular energy sensor, AMP-activated protein kinase (AMPK), via direct phosphorylation. We found that overexpression of vrk-1 in the soma of adult C. elegans increased lifespan, and conversely, inhibition of vrk-1 decreased lifespan. In addition, vrk-1 was required for longevity conferred by mutations that inhibit C. elegans mitochondrial respiration, which requires AMPK. Notably, VRK-1 directly phosphorylated and up-regulated AMPK in both C. elegans and cultured human cells. Thus, our data show that the somatic nuclear kinase, VRK-1, promotes longevity through AMPK activation, and this function appears to be conserved between C. elegans and humans.
2020-07-01 | GSE138129 | GEO
Project description:Hormesis occurs when a low level stress elicits adaptive beneficial responses that protect against subsequent exposure to severe stress. Recent findings suggest that mild oxidative and thermal stress can extend lifespan by hormetic mechanisms. Here we show that the botanical pesticide plumbagin, while toxic to C. elegans nematodes at high doses, extends lifespan at low doses. Because plumbagin is a naphthoquinone that generates free radicals in vivo, we investigated whether it extends lifespan by activating an adaptive cellular stress response pathway. Mammalian NF-E2-related factor 2 (Nrf2) and its C. elegans ortholog SKN-1, mediate protective responses to oxidative stress by promoting target gene expression via antioxidant response elements (ARE). Genetic analyses showed that skn-1 mediates plumbagin’s lifespan-extending effect in C. elegans. Further screening of a series of plumbagin analogs identified three additional naphthoquinones that could induce SKN-1 targets in C. elegans. Naphthazarin showed skn-1-dependent lifespan extension, over an extended dose range compared to plumbagin, while the other naphthoquinones, oxoline and menadione, had differing effects on C. elegans survival and failed to activate ARE reporter expression in cultured mammalian cells. Our findings reveal the potential for low doses of naturally occurring naphthoquinones to extend lifespan by engaging a specific adaptive cellular stress response pathway.
2012-03-21 | GSE28301 | GEO