Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274976 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1793991.fastq.gz | Fastqsanger.gz | |||
| SRR1793992.fastq.gz | Fastqsanger.gz | |||
| SRR1793993.fastq.gz | Fastqsanger.gz | |||
| SRR1793994.fastq.gz | Fastqsanger.gz |
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Project description:Probiotics play important role in maintaining the health and extend longevity in their host. Previous studies reported several live probiotic bacteria in enhancing longevity and improving diverse feature of the host’s health. In this study, we reported a new potential heat- killed probiotic bacterium Levilactobacillus brevis strain MRKAK9 improved longevity and different features of healthy aging, including age-associated physical activity, improved resistance to biotic and abiotic stress in C. elegans. The mechanistic investigations showed that heat-killed strain MRKAK9 promoted longevity and healthy aging by downregulating insulin-signaling pathway resulting in improved proteostasis, autophagy and preserving lysosomal functionality in C. elegans. Heat-killed strain MRKAK9-mediated downregulation of insulin signaling pathway was regulated by the miRNA mir-243, suggesting that mir-243 partially involved in enhancing longevity of C. elegans. Additionally, the structural component exopolysaccharide of the strain heat-killed MRKAK9 also downregulated insulin- signaling mechanisms, increased the expression of genes involved in proteostatsis, autophagy as well as improved expression of mir-243. This study indicates that heat-killed strain MRKAK9 improves longevity and healthy aging, suggesting its candidature as a novel postbiotic.
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Project description:Activation of DAF-16/FOXO by reactive oxygen species promotes longevity in long- lived mitochondrial mutants in C. elegans
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Project description:The transcription elongation factor Spt6 and the H3K36 methyltransferase Set2 are both required for H3K36 methylation and transcriptional fidelity in Saccharomyces cerevisiae. By selecting for suppressors of a transcriptional defect in an spt6 mutant, we have isolated dominant SET2 mutations (SET2sup mutations) in a region encoding a proposed autoinhibitory domain. The SET2sup mutations suppress the H3K36 methylation defect in the spt6 mutant, as well as in other mutants that impair H3K36 methylation. ChIP-seq studies demonstrate that the H3K36 methylation defect in the spt6 mutant, as well as its suppression by a SET2sup mutation, occur at a step following the recruitment of Set2 to chromatin. Other experiments show that a similar genetic relationship between Spt6 and Set2 exists in Schizosaccharomyces pombe. Taken together, our results suggest a conserved mechanism by which the Set2 autoinhibitory domain requires multiple interactions to ensure that H3K36 methylation occurs specifically on actively transcribed chromatin.
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Project description:Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway.
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Project description:Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans
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Project description:Loss of function during ageing is accompanied by transcriptional drift, altering gene expression and contributing to a variety of age-related diseases. CREB-regulated transcriptional coactivators (CRTCs) have emerged as key regulators of gene expression that might be targeted to promote longevity. Here, we define the role of the Caenorhabditis elegans CRTC-1 in the epigenetic regulation of longevity. Endogenous CRTC-1 binds chromatin factors, including components of the COMPASS complex, which trimethylates lysine 4 on histone H3 (H3K4me3). CRISPR editing of endogenous CRTC-1 reveals that the CREB-binding domain in neurons is specifically required for H3K4me3-dependent longevity. However, this effect is independent of CREB but instead acts via the transcription factor AP-1. Strikingly, CRTC-1 also mediates global histone acetylation levels, and this acetylation is essential for H3K4me3-dependent longevity. Indeed, overexpression of an acetyltransferase enzyme is sufficient to promote longevity in wild-type worms. CRTCs, therefore, link energetics to longevity by critically fine-tuning histone acetylation and methylation to promote healthy ageing.
2023-09-26 | PXD045674 | JPOST Repository