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Trichome development is dependent on gibberellin (GA) signaling in Arabidopsis thaliana. Using the GA-deficient mutant ga1-3, the GA-response mutant spy-5, and uniconazol (a GA-biosynthesis inhibitor), we show that the GA level response correlates positively with both trichome number and trichome branch number. Two genes, GL1 and TTG, are required for trichome initiation. In ga1-3, coexpression of GL1 and R, the maize TTG functional homolog, under control of the constitutive 35S promoter, restored trichome development, whereas overexpression of neither GL1 nor R alone was sufficient to significantly suppress the glabrous phenotype. We next focused on GL1 regulation by GAs. In the double mutant the gl1-1 glabrous phenotype is epistatic to the spy-5 phenotype, suggesting that GL1 acts downstream of the GA signal transduction pathway. The activity of a ␤-glucuronidase reporter gene driven by the GL1 promoter was decreased in the wild type grown on uniconazol and showed a clear GA-dependent activation in ga1-3. Finally, quantification of GL1 transcript levels by reverse transcriptase-polymerase chain reaction demonstrated that relative to wild type, ga1-3 plants contained less transcript. These data support the hypothesis that GAs induce trichome development through up-regulation of GL1 and possibly TTG genes.

Embryonic regulators LEC2 (LEAFY COTYLEDON2) and FUS3 (FUSCA3) are involved in multiple aspects of Arabidopsis (Arabidopsis thaliana) seed development, including repression of leaf traits and premature germination and activation of seed storage protein genes. In this study, we show that gibberellin (GA) hormone biosynthesis is regulated by LEC2 and FUS3 pathways. The level of bioactive GAs is increased in immature seeds of lec2 and fus3 mutants relative to wild-type level. In addition, we show that the formation of ectopic trichome cells on lec2 and fus3 embryos is a GA-dependent process as in true leaves, suggesting that the GA pathway is misactivated in embryonic mutants. We next demonstrate that the GA-biosynthesis gene AtGA3ox2, which encodes the key enzyme AtGA3ox2 that catalyzes the conversion of inactive to bioactive GAs, is ectopically activated in embryos of the two mutants. Interestingly, both b-glucuronidase reporter gene expression and in situ hybridization indicate that FUS3 represses AtGA3ox2 expression mainly in epidermal cells of embryo axis, which is distinct from AtGA3ox2 pattern at germination. Finally, we show that the FUS3 protein physically interacts with two RY elements (CATGCATG) present in the AtGA3ox2 promoter. This work suggests that GA biosynthesis is directly controlled by embryonic regulators during Arabidopsis embryonic development.Higher plant embryogenesis is divided into two major phases: embryo development (or morphogenesis) and seed maturation (West and Harada, 1993). During embryo development, early morphogenetic processes occur that give rise to embryonic cell types, tissues, and organs. During seed maturation, the fully developed embryo undergoes maturation, during which food reserves accumulate and dormancy and desiccation tolerance develop.Seed development has been extensively studied in Arabidopsis (Arabidopsis thaliana) using mutants defective either in morphogenesis, such as GNOM (Mayer et al., 1991;Shevell et al., 1994) or KNOLLE (Mayer et al., 1991;Lukowitz et al., 1996), or in maturation, such as ABI (ABSCISIC ACID-INSENSITIVE) loci that were initially identified on the basis of the abscisic acid (ABA) hormone-resistant germination of mutants at these loci (Koornneef et al., 1984;Giraudat et al., 1992;Finkelstein et al., 1998;Finkelstein and Lynch, 2000). A particular set of mutants exhibiting the lec phenotype, which consists of a partial transformation of cotyledons into leaves, has allowed the identification of an important network of regulatory genes. The LEC1 (LEAFY COTYLEDON1; Meinke, 1992), LEC2 (Meinke et al., 1994), and FUS3 (FUSCA3;Keith et al., 1994;Meinke et al., 1994) genes, which are defined as the LEC genes hereafter, are the only known regulators required for normal development during both the morphogenesis and the maturation phases (Holdsworth et al., 1999;Harada, 2001 Article, publication date, and citation information can be found at www.plantphysiol.org/cgi