Genome-wide RNAi Screen for Fat Regulatory Genes in C. elegans Identifies a Proteostasis-AMPK Axis Critical for Starvation Survival
Cell Reports, ISSN: 2211-1247, Vol: 20, Issue: 3, Page: 627-640
2017
- 28Citations
- 81Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations28
- Citation Indexes28
- 28
- CrossRef21
- Captures81
- Readers81
- 81
Article Description
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.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2211124717308999; http://dx.doi.org/10.1016/j.celrep.2017.06.068; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85025100230&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/28723566; https://linkinghub.elsevier.com/retrieve/pii/S2211124717308999; https://dx.doi.org/10.1016/j.celrep.2017.06.068
Elsevier BV
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