A shift of the TOR adaptor from Rictor towards Raptor by semaphorin in C. elegans

Abstract

The target of rapamycin (TOR), a central regulator for cell growth and metabolism, resides in the two functionally distinct complexes TORC1 and TORC2, which are defined by their adaptors Raptor and Rictor, respectively. How the formation of the two TORCs is orchestrated remains unclear. Here we show the control of TOR partnering by semaphorin-plexin signalling in Caenorhabditis elegans. In semaphorin and plexin mutants, TOR-Raptor association decreases whereas TOR-Rictor association increases, concomitantly with TORC1 down- and TORC2 up-regulation. Epidermal defects in the mutants are suppressed by inhibiting TORC2 or reinforcing TORC1 signalling. Conversely, inhibition of TORC1 signalling phenocopies the mutants. Thus, our results indicate that TORC formation is a singularly important step in semaphorin signalling that culminates in diverse outcomes including TORC1-promoted messenger RNA translation and TORC2-regulated cytoskeletal remodelling. What controls the binding partner selection of the target of rapamycin protein, TOR, is unknown. Using theCaenorhabditis elegans tail as a model, Nukazuka et al. determine that signals of semaphorin through plexin control the binding partner selection of TOR and are required for the correct organization of rays in the tail.