SLC7A5 (also known as LAT1), largely accepted as an amino acid transporter, has been shown to play important roles in cancer and developmental process. Because knockout mice of slc7a5 are embryonically lethal due to placental defects, it is difficult to evaluate its role in early development. In this study, slc7a5 expression and function was evaluated in Xenopus laevis embryos that do not require the placenta. Expression of slc7a5 was detected in the notochord and in the eye from gastrula stage and it was not co-localized with slc3a2, which helps slc7a5 to localize at the plasma membrane, before late neurula stage. Loss-of-function experiment with morpholino antisense oligonucleotide led to early neural patterning defect and inhibition of primary neurogenesis. These defects were likely due to impaired notochord development as sonic hedgehog (shh) signaling pathway was compromised in slc7a5-inhibited embryos. These results suggest that slc7a5 is required for notochord development and subsequent neural patterning via shh/gli signaling. In early stages of neural development, the function of slc7a5 appeared to be independent of transport function.