ArticlePLoS genetics2010
Manipulation of behavioral decline in Caenorhabditis elegans with the Rag GTPase raga-1.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
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- Determination of health status during aging using bending and pumping rates at various survival rates in Caenorhabditis elegans.Scientific reports · 2025Article
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- Nutrient control of growth and metabolism through mTORC1 regulation of mRNA splicing.Molecular cell · 2024Article
- Fasting shapes chromatin architecture through an mTOR/RNA Pol I axis.Nature cell biology · 2024Article
- Role of the central nervous system in cell non-autonomous signaling mechanisms of aging and longevity in mammals.The journal of physiological sciences : JPS · 2024Review
- Timing of TORC1 inhibition dictates Pol III involvement inLife science alliance · 2024Article
- Neuronal mTORC1 inhibition promotes longevity without suppressing anabolic growth and reproduction in C. elegans.PLoS genetics · 2023Article
- Ether lipid biosynthesis promotes lifespan extension and enables diverse pro-longevity paradigms ineLife · 2023Article
- Devo-Aging: Intersections Between Development and Aging.GeroScience · 2023Review
- V-ATPase/TORC1-mediated ATFS-1 translation directs mitochondrial UPR activation in C. elegans.The Journal of cell biology · 2023Article
- Stimulation of RAS-dependent ROS signaling extends longevity by modulating a developmental program of global gene expression.Science advances · 2022Article
- Decreased spliceosome fidelity and egl-8 intron retention inhibit mTORC1 signaling to promote longevity.Nature aging · 2022Article
- Coupling of growth rate and developmental tempo reduces body size heterogeneity in C. elegans.Nature communications · 2022Article
- Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- Insights Into the Links Between Proteostasis and Aging FromFrontiers in aging · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal aging leads to an inexorable decline in motor performance, contributing to medical morbidity and decreased quality of life. While much has been discovered about genetic determinants of lifespan, less is known about modifiers of age-related behavioral decline and whether new gene targets may be found which extend vigorous activity, with or without extending lifespan. Using Caenorhabditis elegans, we have developed a model of declining neuromuscular function and conducted a screen for increased behavioral activity in aged animals. In this model, behavioral function suffers from profound reductions in locomotory frequency, but coordination is strikingly preserved until very old age. By screening for enhancers of locomotion at advanced ages we identified the ras-related Rag GTPase raga-1 as a novel modifier of behavioral aging. raga-1 loss of function mutants showed vigorous swimming late in life. Genetic manipulations revealed that a gain of function raga-1 curtailed behavioral vitality and shortened lifespan, while a dominant negative raga-1 lengthened lifespan. Dietary restriction results indicated that a raga-1 mutant is relatively protected from the life-shortening effects of highly concentrated food, while RNAi experiments suggested that raga-1 acts in the highly conserved target of rapamycin (TOR) pathway in C. elegans. Rag GTPases were recently shown to mediate nutrient-dependent activation of TOR. This is the first demonstration of their dramatic effects on behavior and aging. This work indicates that novel modulators of behavioral function can be identified in screens, with implications for future study of the clinical amelioration of age-related decline.
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Registered trials
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.