A study of epidermal morphogenesis regulated by semaphorin signaling

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The target of rapamycin (TOR) 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. Through our study in C. elegans, we demonstrated the control of TOR partnering by semaphorin-plexin signaling in vivo. 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 semaphorin and plexin mutants are suppressed by inhibiting TORC2 or reinforcing TORC1 signaling. Conversely, inhibition of TORC1 signaling phenocopies semaphorin and plexin mutants. Our results indicate that TORC formation is a singularly important step in semaphorin signaling that culminates in diverse outcomes including TORC1-promoted mRNA translation and TORC2-regulated cytoskeletal remodeling.