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GTP ase ROP 2 binds and promotes activation of target of rapamycin, TOR , in response to auxin
Author(s) -
Schepetilnikov Mikhail,
Makarian Joelle,
Srour Ola,
Geldreich Angèle,
Yang Zhenbiao,
Chicher Johana,
Hammann Philippe,
Ryabova Lyubov A
Publication year - 2017
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201694816
Subject(s) - library science , biology , humanities , art , computer science
Target of rapamycin ( TOR ) promotes reinitiation at upstream ORF s (u ORF s) in genes that play important roles in stem cell regulation and organogenesis in plants. Here, we report that the small GTP ase ROP 2, if activated by the phytohormone auxin, promotes activation of TOR , and thus translation reinitiation of u ORF ‐containing mRNA s. Plants with high levels of active ROP 2, including those expressing constitutively active ROP 2 ( CA ‐ ROP 2), contain high levels of active TOR . ROP 2 physically interacts with and, when GTP ‐bound, activates TOR in vitro . TOR activation in response to auxin is abolished in ROP ‐deficient rop2 rop6 ROP4 RNAi plants. GFP ‐ TOR can associate with endosome‐like structures in ROP 2‐overexpressing plants, indicating that endosomes mediate ROP 2 effects on TOR activation. CA ‐ ROP 2 is efficient in loading u ORF ‐containing mRNA s onto polysomes and stimulates translation in protoplasts, and both processes are sensitive to TOR inhibitor AZD ‐8055. TOR inactivation abolishes ROP 2 regulation of translation reinitiation, but not its effects on cytoskeleton or intracellular trafficking. These findings imply a mode of translation control whereby, as an upstream effector of TOR , ROP 2 coordinates TOR function in translation reinitiation pathways in response to auxin.