Trichome development is dependent on gibberellin (CA) signaling in Ara
bidopsis thaliana. Using the CA-deficient mutant ga1-3, the CA-respons
e mutant spy-5, and uniconazol (a GA-biosynthesis inhibitor), we show
that the CA level response correlates positively with both trichome nu
mber and trichome branch number. Two genes, GL1 and TTG, are required
for trichome initiation. In ga1-3, coexpression of GL1 and R, the maiz
e TTG functional homolog, under control of the constitutive 35S promot
er, restored trichome development, whereas overexpression of neither G
L1 nor R alone was sufficient to significantly suppress the glabrous p
henotype. We next focused on GL1 regulation by GAs. In the double muta
nt the gl1-1 glabrous phenotype is epistatic to the spy-5 phenotype, s
uggesting that GL1 acts downstream of the GA signal transduction pathw
ay. The activity of a beta-glucuronidase reporter gene driven by the G
L1 promoter was decreased in the wild type grown on uniconazol and sho
wed a clear GA-dependent activation in ga1-3. Finally, quantification
of GL1 transcript levels by reverse transcriptase-polymerase chain rea
ction demonstrated that relative to wild type, ga1-3 plants contained
less transcript. These data support the hypothesis that GAs induce tri
chome development through up-regulation of GL1 and possibly TTG genes.