Abstract
Stress induces various responses, including translational suppression and tRNA degradation in mammals. Previously, we showed that heat stress induces degradation of initiator tRNAMet (iMet) through 5′-3′ exoribonuclease Xrn1 and Xrn2, respectively. In addition, we found that rapamycin inhibits the degradation of iMet under heat stress conditions. Here, we report that the mammalian target of rapamycin (mTOR) regulates the diffusion of Xrn2 from the nucleolus to the nucleoplasm, facilitating the degradation of iMet under conditions of heat stress. Our results suggest a mechanism of translational suppression through mTOR-regulated iMet degradation in mammalian cells.
Original language | English |
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Pages (from-to) | 3454-3460 |
Number of pages | 7 |
Journal | FEBS Letters |
Volume | 588 |
Issue number | 18 |
DOIs | |
Publication status | Published - Sept 17 2014 |
Keywords
- Heat stress
- Mammalian target of rapamycin
- Xrn2
- tRNA degradation
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology