Ca²⁺, calmodulin, and protein dephosphorylation are required for GA-induced gene expression in petunia corolla

Gibberellic acid (GA₃) induces the expression of different genes, including chalcone synthase (chs) and gip, in detached petunia corollas. To initiate a study on gibberellin (GA)-signal transduction in this tissue, we examined the effect of agents that inhibit or promote specific steps in signal-transduction pathways. The calcium chelator 1,2-bis(o-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA) had no effect on GA-induced gene expression, while the calcium-channel blocker, ruthenium red (RR), inhibited the activation of the genes. The calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) inhibited the induction of chs and gip by the hormone, and its analog, N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride (W-5), had lower effect. The activation of chs and gip by GA₃ was completely blocked by the protein phosphatase inhibitor, okadaic acid (OA), and partially inhibited by the protein kinase inhibitor, 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine dihydrochloride (H-7). We suggest that Ca²⁺ from intracellular sources, calmodulin and protein dephosphorylation and phosphorylation are involved in GA-induced gene expression in petunia corollas.