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Bacillus licheniformis isolated from Korean traditional food resources enhances the lifespan of Caenorhabditis elegans through serotonin signaling

ABSTRACT: 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

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE63056 | GEO | 2015/11/05

SECONDARY ACCESSION(S): PRJNA266520

REPOSITORIES: GEO

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Bacillus licheniformis isolated from Korean traditional food resources enhances the lifespan of Caenorhabditis elegans through serotonin signaling

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

PM2.5 exposure induces lifespan reduction in Caenorhabditis elegans

Project description:To elucidate the molecular mechanism underlying lifespan reduction induced by PM2.5 exposure in Caenorhabditis elegans, we performed global gene expression profiling by RNA-sequencing technology, and compared the gene expression pattern change induced by PM2.5 exposure.

2023-02-22 | GSE214215 | GEO

Glucose Shortens the Lifespan of Caenorhabditis elegans by Down-Regulating Aquaporin Gene Expression

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

Crotamiton derivative JM03 extends lifespan and improves oxidative and hypertonic stress resistance in Caenorhabditis elegans via inhibiting OSM-9

Project description:While screening our in-house 1,072 marketed drugs for their ability to extend the lifespan using Caenorhabditis elegans (C. elegans) as an animal model, crotamiton (N-ethyl-o-crotonotoluidide) showed anti-aging activity and was selected for further structural optimization. After replacing the ortho-methyl of crotamiton with ortho-fluoro, crotamiton derivative JM03 was obtained and showed better activity in terms of lifespan-extension and stress resistance than crotamiton. It was further explored that JM03 extended the lifespan of C. elegans through osmotic avoidance abnormal-9 (OSM-9). Besides, JM03 improves the ability of nematode to resist oxidative stress and hypertonic stress through OSM-9, but not osm-9/capsaicin receptor related-2 (OCR-2). Then the inhibition of OSM-9 by JM03 reduces the aggregation of Q35 in C. elegans via upregulating the genes associated with proteostasis. SKN-1 signaling was also found to be activated after JM03 treatment, which might contribute to proteostasis, stress resistance and lifespan extension. In summary, this study explored a new small molecule derived from crotamiton, which has efficient anti-oxidative, anti-hypertonic and anti-aging effects, and could further lead to promising application prospects.

2022-04-10 | GSE200459 | GEO

Glucose Shortens the Lifespan of Caenorhabditis elegans by Down-Regulating Aquaporin Gene Expression

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. This SuperSeries is composed of the SubSeries listed below.

2010-01-01 | GSE18563 | GEO

Crotamiton derivative JM03 extends lifespan and improves 1 oxidative and hypertonic stress resistance in Caenorhabditis 2 elegans via inhibiting OSM-9

2021-09-17 | GSE184076 | GEO

Loss of miR-83 extends lifespan and affects target gene expression in an age-dependent manner in Caenorhabditis elegans

Project description:We have identified a role of the C. elegans miR-83 in regulating lifespan. mir-83 mutants exhibit an extended lifespan, and its overexpression is sufficient to decrease the prolonged lifespan of the mutants. We observed an upregulation in the expression of sets of miR-83 targets in young mir-83 mutant adults. However, in older mir-83 mutant adults, a different set of genes are upregulated. In vivo assays show that miR-83 regulates expression of a number of targets, including din-1, spp-9 and col-178. We show that daf-16 and din-1 are required for the lifespan extension of mir-83 mutants. The regulation of din-1 by miR-83 during aging results in the differential expression of din-1 targets, such as gst-4 and gst-10. In daf-2 mutants, the expression levels of miR-83 are significantly reduced, as compared to wildtype animals. Our results identify a role of miR-83 in modulating lifespan in C. elegans, and provide molecular insights into its functional mechanism.

2018-12-15 | GSE123862 | GEO

Caenorhabditis elegans

Project description:Bacillus licheniformis isolated from Korean traditional food resources enhances the lifespan of Caenorhabditis elegans through serotonin signaling

| PRJNA266520 | ENA

Gene Expression Profiling Reveals Molecular Patterns Underlying the Lifespan-Extending Effect of Tyrosol in Caenorhabditis elegans

Project description:We have previously reported that tyrosol (TYR), one of the main phenols in extra virgin olive oil (EVOO), promotes lifespan extension in the nematode Caenorhabditis elegans, also inducing a stronger resistance to thermal and oxidative stress in this animal model. Although the influence of several longevity-related genes in these effects has been reported by our group, we decided to perform a whole genome DNA-microarray approach in order to identify other genes and molecular pathways further involved in TYR effects on C. elegans longevity. Microarray analysis identified 208 differentially expressed genes (206 overexpressed and 2 underexpressed) when comparing TYR-treated nematodes with non-treated controls. Many of these genes seem linked to processes such as regulation of growth, transcription, reproduction, lipid metabolism and body morphogenesis. Data obtained by microarray was validated by qRT-PCR analysis of selected genes. Our results confirm that several important cellular mechanisms related to longevity are influenced by TYR treatment in this animal model. Moreover, we detected an interesting overlap between the expression pattern elicited by TYR and those induced by other dietary polyphenols known to extend lifespan in C. elegans, such as quercetin and tannic acid.

2014-11-01 | GSE57664 | GEO

GNPS - Serotonin biosynthesis and metabolism in C. elegans

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

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