We first cloned Xenopus Rheb, which is generally believed as the upstream positive regulator of TOR, then created dominant negative form of Rheb (dn-Rheb), and also designed antisense morpholino oligomers of Rheb (Rheb-MO). Gain-of-functional experiment of TOR signal by microinjection of Rheb mRNA into blastomeres led the posterior defects for the embryos. FKBP38 is the direct negative regulator of TOR, so FKBP38-MO was also designed. Similar to the case of Rheb mRNA, FKBP38-MO injected embryos lost posterior structures. On the other hand, loss-offunctional experiment by microinjection of dn-Rheb or RhebMO into dorsal blastomeres strongly reduced the size of head structure, and no additional posterior structures were observed. Taken together with these results, we conclude that anteroposterior positional value of Xenopus early development is determined by the level of TOR signal. We also did loss-of-functional experiment of TOR signal using rapamycin that directly binds to TOR and inhibit its activity. Interestingly, rapamycin treated embryos were losing pigmentation derived from neural crest and pronephros with unusual stomach and gut formation, which is also reported in zebrafish studies.