ArticleCell reports2017
Genome-wide RNAi Screen for Fat Regulatory Genes in C. elegans Identifies a Proteostasis-AMPK Axis Critical for Starvation Survival.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
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- Quantifying Food Intake in Caenorhabditis elegans by Measuring Bacterial Clearance.Journal of visualized experiments : JoVE · 2024Article
- Maternal aging increases offspring adult body size via transmission of donut-shaped mitochondria.Cell research · 2023Article
- Changes in lipid metabolism driven by steroid signalling modulate proteostasis in C. elegans.EMBO reports · 2023Article
- Lipid droplets and peroxisomes are co-regulated to drive lifespan extension in response to mono-unsaturated fatty acids.Nature cell biology · 2023Article
- Application ofInternational journal of molecular sciences · 2023Review
- Cytoplasmic and mitochondrial aminoacyl-tRNA synthetases differentially regulate lifespan iniScience · 2022Article
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- Engineering immunoproteasome-expressing mesenchymal stromal cells: A potent cellular vaccine for lymphoma and melanoma in mice.Cell reports. Medicine · 2021Article
- mmBCFA C17iso ensures endoplasmic reticulum integrity for lipid droplet growth.The Journal of cell biology · 2021Article
- Serum- and glucocorticoid-induced kinase drives hepatic insulin resistance by directly inhibiting AMP-activated protein kinase.Cell reports · 2021Article
- Genes in human obesity loci are causal obesity genes in C. elegans.PLoS genetics · 2021Article
- Article
- Starvation Responses Throughout theGenetics · 2020Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Organisms must execute metabolic defenses to survive nutrient deprivation. We performed a genome-wide RNAi screen in Caenorhabditis elegans to identify fat regulatory genes indispensable for starvation resistance. Here, we show that opposing proteostasis pathways are principal determinants of starvation survival. Reduced function of cytoplasmic aminoacyl tRNA synthetases (ARS genes) increases fat mass and extends starvation survival, whereas reduced proteasomal function reduces fat and starvation survival. These opposing pathways converge on AMP-activated protein kinase (AMPK) as the critical effector of starvation defenses. Extended starvation survival in ARS deficiency is dependent upon increased proteasome-mediated activation of AMPK. When the proteasome is inhibited, neither starvation nor ARS deficiency can fully activate AMPK, leading to greatly diminished starvation survival. Thus, activity of the proteasome and AMPK are mechanistically linked and highly correlated with starvation resistance. Conversely, aberrant activation of the proteostasis-AMPK axis during nutritional excess may have implications for obesity and cardiometabolic diseases.
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