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mTOR regulates the nucleoplasmic diffusion of Xrn2 under conditions of heat stress
Author(s) -
Watanabe Kazunori,
Ijiri Kenichi,
Ohtsuki Takashi
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.08.003
Subject(s) - nucleolus , pi3k/akt/mtor pathway , microbiology and biotechnology , nucleoplasm , chemistry , autophagy , stress granule , degradation (telecommunications) , biology , biochemistry , signal transduction , messenger rna , translation (biology) , cytoplasm , gene , apoptosis , telecommunications , computer science
Stress induces various responses, including translational suppression and tRNA degradation in mammals. Previously, we showed that heat stress induces degradation of initiator tRNA Met (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.