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Role of JNK in global translation under normal growth conditions
Author(s) -
Ito Masatoshi,
Kitamura Hiroshi,
Kikuguchi Chisato,
Yuasa Tomoko,
Ohno Hiroshi,
Ohara Osamu
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.319
Subject(s) - internal ribosome entry site , translation (biology) , phosphorylation , pi3k/akt/mtor pathway , protein biosynthesis , kinase , messenger rna , small hairpin rna , microbiology and biotechnology , translational regulation , biology , rna , chemistry , signal transduction , biochemistry , gene
Whereas c‐Jun N‐terminal Kinase (JNK) is required for translation of certain transcripts under stressed situations, little is known about its role in translation under normal growth conditions. In mouse macrophage‐like J774.1 cells, we found that a JNK inhibitor SP600125 (SP) induced a 40% decrement of nascent protein production. In agreement with this, SP treatment caused 30% decrement of polysomal RNAs and 20% increment of non‐polysomal ones. On the other hand, RNA blotting analysis showed that amounts of randomly selected 11 transcripts were decreased in polysomal fractions by SP treatment, implying SP‐induced translational suppression globally happened in the cell. Since shRNA for JNK1 also reduced nascent protein productivity in J774.1 cells, JNK1 seems to be responsible for suppression of global translation. Because the phosphorylated forms of AKT, mTOR, and S6kinase disappeared after SP treatment, JNK might be involved in control of cap‐dependent translation. In addition, internal ribosome entry site (IRES)‐containing transcripts such as transcripts for p27Kip1 and ornithine decarboxylase were also translationally suppressed by SP treatment, suggesting JNK was also involved in control of IRES‐dependent translation. Taken these results together, we concluded that JNK participated in global translation via both cap‐ and IRES‐mediated mechanisms under normal growth conditions.