Insulin Signaling Augments eIF4E-Dependent Nonsense-Mediated mRNA Decay in Mammalian Cells
- Authors
- Park, Jungyun; Ahn, Seyoung; Jayabalan, Aravinth K.; Ohn, Takbum; Koh, Hyun Chul; Hwang, Jungwook
- Issue Date
- Jul-2016
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- PI3K/AKT/mTOR; Insulin; NMD; Translation; Processing body
- Citation
- BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, v.1859, no.7, pp.896 - 905
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
- Volume
- 1859
- Number
- 7
- Start Page
- 896
- End Page
- 905
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/154311
- DOI
- 10.1016/j.bbagrm.2015.12.006
- ISSN
- 1874-9399
- Abstract
- Nonsense-mediated mRNA decay (NMD) modulates the level of mRNA harboring a premature termination codon (PTC) in a translation-dependent manner. Inhibition of translation is known to impair NMD; however, few studies have investigated the correlation between enhanced translation and increased NMD. Here, we demonstrate that insulin signaling events increase translation, leading to an increase in NMD of eIF4E-bound transcripts. We provide evidence that (i) insulin-mediated enhancement of translation augments NMD and rapamycin abrogates this enhancement; (ii) an increase in AKT phosphorylation due to inhibition of PTEN facilitates NMD; (iii) insulin stimulation increases the binding of up-frameshift factor 1 (UPF1), most likely to eIF4E-bound PTC-containing transcripts; and (iv) insulin stimulation induces the colocalization of UPF1 and eIF4E in processing bodies. These results illustrate how extracellular signaling promotes the removal of eIF4E-bound NMD targets.
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