ArticleCell metabolism2016
Reversible Age-Related Phenotypes Induced during Larval Quiescence in C. elegans.
Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 81 citations in OpenAlex.
- HLH-30/TFEB is necessary for chromatin reorganization and maintenance of cell quiescence during starvation in C. elegans.Nucleic acids research · 2026Article
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- Fasting requires Peroxiredoxin 2 and Peroxiredoxin 6 to coordinate redox dependent mitochondrial and lipid remodelling in Caenorhabditis elegans.Redox biology · 2026Article
- MAK-2 Kinase Is Required for Extended Longevity and Enhanced Stress Resistance Resulting From Mild Impairment of Mitochondrial Function in isp-1 Mutants.Aging cell · 2026Article
- Computational Approaches to Cancer Cell Dormancy: From Detection to Dynamic Modelling.Biomolecules · 2026Review
- Age Deceleration and Reversal Gene Patterns in Dauer Diapause.Aging cell · 2025Article
- ATG-3 limits Orsay virus infection in C. elegans and regulates collagen pathways.PLoS pathogens · 2025Article
- A paradoxical role of autophagy: promoting protein aggregates and hindering rejuvenation in aAutophagy · 2025Article
- Doxifluridine promotes host longevity through bacterial metabolism.PLoS genetics · 2025Article
- Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans.Nature communications · 2025Article
- Article
- Decoding aging: examining the non-evolutionary event from an evolutionary perspective.Science China. Life sciences · 2024Article
- A sleep-active neuron can promote survival while sleep behavior is disturbed.PLoS genetics · 2023Article
- The metabolite alpha-ketobutyrate extends lifespan by promoting peroxisomal function in C. elegans.Nature communications · 2023Article
- Mitochondrial genome recovery by ATFS-1 is essential for development after starvation.Cell reports · 2022Article
- Alternative somatic and germline gene-regulatory strategies during starvation-induced developmental arrest.Cell reports · 2022Article
- Using population selection and sequencing to characterize natural variation of starvation resistance ineLife · 2022Article
- Coupling of growth rate and developmental tempo reduces body size heterogeneity in C. elegans.Nature communications · 2022Article
- Hijacking Cellular Stress Responses to Promote Lifespan.Frontiers in aging · 2022Review
- Inactivation of theAutophagy · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cells can enter quiescent states in which cell cycling and growth are suspended. We find that during a long developmental arrest (quiescence) induced by starvation, newly hatched C. elegans acquire features associated with impaired proteostasis and aging: mitochondrial fission, ROS production, protein aggregation, decreased proteotoxic-stress resistance, and at the organismal level, decline of mobility and high mortality. All signs of aging but one, the presence of protein aggregates, were reversed upon return to development induced by feeding. The endoplasmic reticulum receptor IRE-1 is completely required for recovery, and the downstream transcription factor XBP-1, as well as a protein kinase, KGB-1, are partially required. Interestingly, kgb-1(-) mutants that do recover fail to reverse aging-like mitochondrial phenotypes and have a short adult lifespan. Our study describes the first pathway that reverses phenotypes of aging at the exit of prolonged quiescence.
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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.