Ectopic expression of the Arabidopsis florigen gene FLOWERING LOCUS T in seeds enhances seed dormancy via the GA and DOG1 pathways

SUMMARY Ectopic expression of specific genes in seeds could be a tool for molecular design of crops to alter seed dormancy and germination, thereby improving production. Here, a seed‐specific vector, 12S‐pLEELA, was applied to study the roles of genes in Arabidopsis seeds. Transgenic lines containing FLOWERING LOCUS T ( FT ) driven by the 12S promoter exhibited significantly increased seed dormancy and earlier flowering. Mutated FT(Y85H) and TERMINAL FLOWER1 (TFL1) transgenic lines also showed increased seed dormancy but without altered flowering time. FT(Y85H) and TFL1 caused weaker seed dormancy enhancement compared to FT. The FT and TFL1 transgenic lines showed hypersensitivity to paclobutrazol, but not to abscisic acid in seed germination. The levels of bioactive gibberellin 3 (GA 3 ) and GA 4 were significantly reduced, consistent with decreased expression of COPALYL DIPHOSPHATE SYNTHASE ( CPS ), KAURENE OXIDASE ( KO ), GIBBERELLIN 3‐OXIDASE2 ( GA3ox2 ), and GA20ox1 in p12S::FT lines. Exogenous GA 4+7 could recover the germination ability of FT transgenic lines. These results revealed that FT regulates GA biosynthesis. A genetic analysis indicated that the GA signaling regulator SPINDLY (SPY) is epistatic to FT in GA‐mediated seed germination. Furthermore, DELAY OF GERMINATION1 ( DOG1 ) showed significantly higher transcript levels in p12S::FT lines. Seed dormancy analysis of dog1‐2 spy‐3 p12S::FT‐2 indicated that the combination of SPY and DOG1 is epistatic to FT in the regulation of dormancy. Overall, we showed that ectopic expression of FT and TFL1 in seeds enhances dormancy through affecting GA and DOG1 pathways.