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Polarity along the adaxial–abaxial axis of the leaf is essential for leaf development and morphogenesis. One of the genes that encodes a putative transcription factor regulating adaxial–abaxial polarity, FILAMENTOUS FLOWER (FIL), is expressed in the abaxial region of the leaf primordia. However, the molecular mechanisms controlling the polarized expression of FIL remain unclear. Here, we analyzed an enlarged fil expression domain1 (enf1) mutant of Arabidopsis, which forms both abaxialized leaves and adaxialized leaves. The ENF1 gene encodes SUCCINIC SEMIALDEHYDE DEHYDROGENASE (SSADH), which catalyzes the conversion of succinic semialdehyde (SSA) to succinate. The enf1 phenotype was suppressed by an additional mutation in GAMMA-AMINOBUTYRIC ACID AMINOTRANSFERASE1 (GABAT1), which encodes an SSA-producing enzyme, suggesting that SSA or its derivatives is the metabolite responsible for the defect in the adaxial–abaxial axis-dependent gene expression of enf1. In the shoot apical meristem, GABAT1 was expressed in the outermost layer but SSADH was not. Exogenous application of SSA induced adaxial characters on the abaxial side of the newly developed leaves. We suggest that a GABA shunt metabolite, SSA or its close derivatives, is involved in the robust leaf patterning and structure along the adaxial–abaxial axis. [ABSTRACT FROM AUTHOR]