ArticlePLoS genetics2018
Hypodermal responses to protein synthesis inhibition induce systemic developmental arrest and AMPK-dependent survival in Caenorhabditis elegans.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
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- Maternal regulation of translation capacity across generations.PLoS biology · 2026Article
- Cycloheximide-resistant ribosomes reveal adaptive translation dynamics in C. elegans.Genetics · 2026Article
- Depletion of tryptophanyl-tRNA synthetase and tryptophan accumulation triggers p53-dependent apoptosis.Cell death discovery · 2025Article
- Intercellular sphingolipid signaling mediates aversive learning in C. elegans.Current biology : CB · 2025Article
- A role for BYN-1/bystin in cellular uptake and clearance of residual bodies in the Caenorhabditis elegans germline.Development (Cambridge, England) · 2024Article
- Serotonin deficiency from constitutive SKN-1 activation drives pathogen apathy.Nature communications · 2024Article
- Tryptophanyl-tRNA synthetase-1 (WARS-1) depletion and high tryptophan concentration lead to genomic instability in Caenorhabditis elegans.Cell death discovery · 2024Article
- A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Comparative analysis of the molecular and physiological consequences of constitutive SKN-1 activation.GeroScience · 2023Article
- Inhibition of ribosome biogenesis in the epidermis is sufficient to trigger organism-wide growth quiescence independently of nutritional status in C. elegans.PLoS biology · 2023Article
- The Caenorhabditis elegans anchor cell transcriptome: ribosome biogenesis drives cell invasion through basement membrane.Development (Cambridge, England) · 2023Article
- Genetic factors in methylmercury-induced neurotoxicity: What have we learned fromAdvances in neurotoxicology · 2023Article
- Fzr regulates silk gland growth by promoting endoreplication and protein synthesis in the silkworm.PLoS genetics · 2023Article
- Different methods of killing bacteria diets differentially influencemicroPublication biology · 2023Article
- Comprehensive proteomic analysis of exosome mimetic vesicles and exosomes derived from human umbilical cord mesenchymal stem cells.Stem cell research & therapy · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- Oolonghomobisflavans from Camellia sinensis increase Caenorhabditis elegans lifespan and healthspan.GeroScience · 2022Article
- Control of aging by the renin-angiotensin system: a review ofFrontiers in pharmacology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Across organisms, manipulation of biosynthetic capacity arrests development early in life, but can increase health- and lifespan post-developmentally. Here we demonstrate that this developmental arrest is not sickness but rather a regulated survival program responding to reduced cellular performance. We inhibited protein synthesis by reducing ribosome biogenesis (rps-11/RPS11 RNAi), translation initiation (ifg-1/EIF3G mutation and egl-45/EIF3A RNAi), or ribosome progression (cycloheximide treatment), all of which result in a specific arrest at larval stage 2 of C. elegans development. This quiescent state can last for weeks-beyond the normal C. elegans adult lifespan-and is reversible, as animals can resume reproduction and live a normal lifespan once released from the source of protein synthesis inhibition. The arrest state affords resistance to thermal, oxidative, and heavy metal stress exposure. In addition to cell-autonomous responses, reducing biosynthetic capacity only in the hypodermis was sufficient to drive organism-level developmental arrest and stress resistance phenotypes. Among the cell non-autonomous responses to protein synthesis inhibition is reduced pharyngeal pumping that is dependent upon AMPK-mediated signaling. The reduced pharyngeal pumping in response to protein synthesis inhibition is recapitulated by exposure to microbes that generate protein synthesis-inhibiting xenobiotics, which may mechanistically reduce ingestion of pathogen and toxin. These data define the existence of a transient arrest-survival state in response to protein synthesis inhibition and provide an evolutionary foundation for the conserved enhancement of healthy aging observed in post-developmental animals with reduced biosynthetic capacity.
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