ArticleMechanisms of ageing and development2016
C. elegans lifespan extension by osmotic stress requires FUdR, base excision repair, FOXO, and sirtuins.
Article in Mechanisms of ageing and development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
54 citing papers in PubMed, 84 citations in OpenAlex.
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- Tauroursodeoxycholic acid targets HSP90 to promote protein homeostasis and extends healthy lifespan.Science China. Life sciences · 2025Article
- Chemotaxis in C. elegans: Interrogating the Effects of Odorants on Physiology.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Floxuridine supports UPS independent of germline signaling and proteostasis regulators via involvement of detoxification in C. elegans.PLoS genetics · 2024Article
- Cacao Procyanidins-Induced Lifespan Extension in Caenorhabditis elegans in a Nervous System and CaMKII-Dependent Manner.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
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- The unfolded protein response reverses the effects of glucose on lifespan in chemically-sterilized C. elegans.Nature communications · 2022Article
- Transcriptomic Analysis in Marine Medaka Gill Reveals That the Hypo-Osmotic Stress Could Alter the Immune Response via the IL17 Signaling Pathway.International journal of molecular sciences · 2022Article
- Serotonin and dopamine modulate aging in response to food odor and availability.Nature communications · 2022Article
- Neuropeptidergic regulation of compulsive ethanol seeking in C. elegans.Scientific reports · 2022Article
- Review
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Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Moderate stress can increase lifespan by hormesis, a beneficial low-level induction of stress response pathways. 5'-fluorodeoxyuridine (FUdR) is commonly used to sterilize Caenorhabditis elegans in aging experiments. However, FUdR alters lifespan in some genotypes and induces resistance to thermal and proteotoxic stress. We report that hypertonic stress in combination with FUdR treatment or inhibition of the FUdR target thymidylate synthase, TYMS-1, extends C. elegans lifespan by up to 30%. By contrast, in the absence of FUdR, hypertonic stress decreases lifespan. Adaptation to hypertonic stress requires diminished Notch signaling and loss of Notch co-ligands leads to lifespan extension only in combination with FUdR. Either FUdR treatment or TYMS-1 loss induced resistance to acute hypertonic stress, anoxia, and thermal stress. FUdR treatment increased expression of DAF-16 FOXO and the osmolyte biosynthesis enzyme GPDH-1. FUdR-induced hypertonic stress resistance was partially dependent on sirtuins and base excision repair (BER) pathways, while FUdR-induced lifespan extension under hypertonic stress conditions requires DAF-16, BER, and sirtuin function. Combined, these results demonstrate that FUdR, through inhibition of TYMS-1, activates stress response pathways in somatic tissues to confer hormetic resistance to acute and chronic stress. C. elegans lifespan studies using FUdR may need re-interpretation in light of this work.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.