作者: Asier González , Mitsugu Shimobayashi , Tobias Eisenberg , David Adrian Merle , Tobias Pendl
DOI: 10.1371/JOURNAL.PONE.0120250
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摘要: The target of rapamycin complex 1 (TORC1) is an evolutionarily conserved sensor nutrient availability. Genetic and pharmacological studies in the yeast Saccharomyces cerevisiae have provided mechanistic insights on regulation TORC1 signaling response to nutrients. Using a highly specific antibody that recognizes phosphorylation bona fide ribosomal protein S6 (Rps6) yeast, we found nutrients rapidly induce Rps6 TORC1-dependent manner. Moreover, demonstrate Ypk3, AGC kinase which exhibits high homology human (S6K), required for vivo. completely abolished cells lacking Ypk3 (ypk3Δ), whereas Sch9, previously reported be ortholog S6K, dispensable phosphorylation. Phosphorylation-deficient mutations regulatory motifs abrogate phosphorylation, complementation ypk3Δ with restores rapamycin-sensitive Our findings critical component pathway use phospho-S6 offers valuable tool identify new nutrient-dependent targets