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RNA surveillance via nonsense-mediated mRNA decay is crucial for longevity in daf-2/insulin/IGF-1 mutant C. elegans

Title
RNA surveillance via nonsense-mediated mRNA decay is crucial for longevity in daf-2/insulin/IGF-1 mutant C. elegans
Authors
Son, Heehwa G.Seo, MihwaHam, SeokjinHwang, WooseonLee, DongyeopAn, Seon Woo A.Artan, MuratSeo, KeunheeKaletsky, RachelArey, Rachel N.Ryu, YoungjaeHa, Chang ManKim, Yoon KiMurphy, Coleen T.Roh, Tae-YoungNam, Hong GilLee, Seung-Jae V.
DGIST Authors
Nam, Hong Gil
Issue Date
2017-03-09
Citation
Nature Communications, 8
Type
Article
Article Type
Article
Keywords
Amyotrophic Lateral SclerosisCaenorhabditis ElegansCaenorhabditis ElegansDAF 16/FOXOExpression AnalysisFrontotemporal Lobar DegenerationNMDPathwaySEQTDP 43Animalia
ISSN
2041-1723
Abstract
Long-lived organisms often feature more stringent protein and DNA quality control. However, whether RNA quality control mechanisms, such as nonsense-mediated mRNA decay (NMD), which degrades both abnormal as well as some normal transcripts, have a role in organismal aging remains unexplored. Here we show that NMD mediates longevity in C. Elegans strains with mutations in daf-2/insulin/insulin-like growth factor 1 receptor. We find that daf-2 mutants display enhanced NMD activity and reduced levels of potentially aberrant transcripts. NMD components, including smg-2/UPF1, are required to achieve the longevity of several long-lived mutants, including daf-2 mutant worms. NMD in the nervous system of the animals is particularly important for RNA quality control to promote longevity. Furthermore, we find that downregulation of yars-2/tyrosyl-tRNA synthetase, an NMD target transcript, by daf-2 mutations contributes to longevity. We propose that NMD-mediated RNA surveillance is a crucial quality control process that contributes to longevity conferred by daf-2 mutations. © The Author(s) 2017.
URI
http://hdl.handle.net/20.500.11750/4220
DOI
10.1038/ncomms14749
Publisher
Nature Publishing Group
Related Researcher
Files:
There are no files associated with this item.
Collection:
New BiologyETC1. Journal Articles


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