Gibberellic acid (GA) plays a key role in seed germination through coordinate interactions with other growth hormones and external signals. However, the way in which external signals are incorporated into the GA-signaling pathway is largely unknown. Here, we demonstrate that a membrane-bound NAC transcription factor NTL8 mediates the salt regulation of seed germination via the GA pathway, primarily independently of ABA. NTL8 is induced by high salinity. Its expression is also elevated by a GA biosynthetic inhibitor paclabutrazol (PAC), but is repressed by GA. Notably, high salinity greatly represses the GA3 oxidase 1 (GA3ox1) gene, supporting the hypothesis that salt signals inhibit seed germination by repressing GA biosynthesis. Induction of NTL8 and repression of GA3ox1 by high salinity still occur in the ABA-deficient aba3-1 mutant. Accordingly, the germination of a T-DNA insertional ntl8-1 mutant seed is resistant to high salinity and PAC. Interestingly, NTL8 is significantly induced during cold imbibition, but the induction declines quickly in germinating seeds, like RGL2. NTL8 activity is also regulated by controlled proteolytic release of the membrane-bound NTL8 form. Its release from the membranes is activated by PAC and high salinity. Our data support that NTL8 modulates GA-mediated salt signaling in regulating seed germination. This regulatory scheme may provide an adaptative fitness, which delays seed germination under high salinity conditions.