• Journal of Microbiology and Biotechnology
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• 제24권9호
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• pp.1269-1279
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• 2014

Xanthomonas oryzae pv. oryzae (Xoo) strains are plant pathogenic bacteria that can cause serious blight of rice, and their virulence towards plant host is complex, making it difficult to be elucidated. Caenorhabditis elegans has been used as a powerful model organism to simplify the host and pathogen system. However, whether the C. elegans is feasible for studying plant pathogens such as Xoo has not been explored. In the present work, we report that Xoo strains PXO99 and JXOIII reduce the lifespan of worms not through acute toxicity, but in an infectious manner; pathogens proliferate and persist in the intestinal lumen to cause marked anterior intestine distension. In addition, Xoo triggers (i) the p38 MAPK signal pathway to upregulate its downstream C17H12.8 expression, and (ii) the DAF-2/DAF-16 pathway to upregulate its downstream gene expressions of mtl-1 and sod-3 under the condition of daf-2 mutation. Our findings suggest that C. elegans can be used as a model to evaluate the virulence of Xoo phytopathogens to host.

• Natural Product Sciences
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• 제22권3호
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• pp.201-208
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• 2016

Here in this study, we investigated the lifespan-extending effect and underlying mechanism of methanolic extract of Moringa olelifa leaves (MML) using Caenorhabditis elegans (C. elegans) model system. To define the longevity properties of MML we conducted lifespan assay and MML showed significant increase in lifespan under normal culture condition. In addition, MML elevated stress tolerance of C. elegans to endure against thermal, oxidative and osmotic stress conditions. Our data also revealed that increased activities of antioxidant enzymes and expressions of stress resistance proteins were attributed to MML-mediated enhanced stress resistance. We further investigated the involvement of MML on the aging-related factors such as growth, food intake, fertility, and motility. Interestingly, MML significantly reduced growth and egg-laying, suggesting these factors were closely linked with MML-mediated longevity. We also observed the movement of aged worms to estimate the effects of MML on the health span. Herein, MML efficiently elevated motility of aged worms, indicating MML may affect health span as well as lifespan. Our genetic analysis using knockout mutants showed that lifespan-extension activity of MML was interconnected with several genes such as skn-1, sir-2.1, daf-2, age-1 and daf-16. Based on these results, we could conclude that MML prolongs the lifespan of worms via activation of SKN-1 and SIR-2.1 and inhibition of insulin/IGF pathway, followed by DAF-16 activation.

• Molecules and Cells
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• 제37권1호
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• pp.51-57
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• 2014

NOG1 is a nucleolar GTPase that is critical for 60S ribosome biogenesis. Recently, NOG1 was identified as one of the downstream regulators of target of rapamycin (TOR) in yeast. It is reported that TOR is involved in regulating lifespan and fat storage in Caenorhabditis elegans. Here, we show that the nog1 ortholog (T07A9.9: nog-1) in C. elegans regulates growth, development, lifespan, and fat metabolism. A green fluorescence protein (GFP) promoter assay revealed ubiquitous expression of C. elegans nog-1 from the early embryonic to the adult stage. Furthermore, the GFP-tagged NOG-1 protein is localized to the nucleus, whereas the aberrant NOG-1 protein is concentrated in the nucleolus. Functional studies of NOG-1 in C. elegans further revealed that nog-1 knockdown resulted in smaller broodsize, slower growth, increased life span, and more fat storage. Moreover, nog-1 over-expression resulted in decreased life span. Taken together, our data suggest that nog-1 in C. elegans may be an important player in regulating life span and fat storage via the insulin/IGF pathway.

• BMB Reports
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• 제52권4호
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• pp.265-270
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• 2019

We investigated whether SIRT1 is associated with reactive oxygen species (ROS) accumulation during CK2 downregulation-mediated senescence. SIRT1 overexpression suppressed ROS accumulation, reduced transcription of FoxO3a target genes, and nuclear export and acetylation of FoxO3a, which were induced by CK2 downregulation in HCT116 and MCF-7 cells. Conversely, overexpression of a dominant-negative mutant SIRT1 (H363Y) counteracted decreased ROS levels, increased transcriptional activity of FoxO3a, and increased nuclear import and decreased acetylation of FoxO3a, which were induced by CK2 upregulation. CK2 downregulation destabilized SIRT1 protein via an ubiquitin-proteasome pathway in human cells, whereas CK2 overexpression reduced ubiquitination of SIRT1. Finally, the SIRT1 activator resveratrol attenuated the accumulation of ROS and lipofuscin as well as lifespan shortening, and reduced expression of the DAF-16 target gene sod-3, which were induced by CK2 downregulation in nematodes. Altogether, this study demonstrates that inactivation of the SIRT1-FoxO3a axis, at least in part, is involved in ROS generation during CK2 downregulation-mediated cellular senescence and nematode aging.

• 생약학회지
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• 제48권3호
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• pp.179-186
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• 2017

Pyrrosia lingua which belongs to Polypodiaceae has been used as a traditional medicine for the treatment of urinary system inflammation, urination disorder, and bronchitis. However, there are not enough phytochemical and pharmacological studies of P. lingua up to now. Here in this study, the protective effect of MeOH extract of whole plant of Pyrrosia lingua (MPL) against 2% glucose-induced toxicity was investigated using Caenorhabditis elegans (C. elegans) model system. We found that MPL significantly extended the lifespan of wild-type nematode under normal culture condition. MPL also effectively recovered the decreased lifespan caused by 2% glucose-toxicity. In addition, MPL efficiently attenuated the increased glucose concentration inside of nematode. Further studies evaluating diabetes-related factors revealed that MPL reduced both intracellular ROS and lipid accumulation which were up-regulated under 2% glucose supplement condition. Our data also showed that MPL improved the 2% glucose-induced shortened body movement of nematode. Lastly, we carried out genetic studies using several single gene knockout mutants to establish the possible target of MPL. Our results demonstrated that genes such as daf-2 and daf-16 were responsible for the protective activity of MPL against 2% glucose-induced toxicity. These results indicate that MPL exerts protective action against 2% glucose via regulation of insulin/IGF-1 sinaling pathway and FOXO activation.