Controlling Plant Architecture by Manipulation of Gibberellic Acid Signaling

A common problem in the production of ornamental potted plants is their undesirably tall growth habit. Growth retardants that are most commonly used to control plant height include A-rest (ancymidol), B-nine (daminozide), Bonzi (paclobutrazol), Cycocel (chlormequat chloride), and Sumagic (uniconazole), all inhibitors of gibberellic acid (GA) biosynthesis. Given the high cost, potential environmental impact and possible phytotoxicity of these chemicals, we investigated interfering with GA signaling as an alternative approach. GA is thought to bind to a soluble GID1 receptor, which in turn binds to the DELLA repressor protein. The bound DELLA protein is then targeted for degradation by the proteasome, thus relieving DELLA-mediated repression of GA-dependent growth processes. To control plant height, we propose to interrupt GA signaling either by silencing receptor genes or by stabilizing the DELLA repressor. We have isolated three putative GID1 genes (PhGID1A, PhGID1B, and PhGID1C) from petunia. Virus-induced gene silencing (VIGS) of these genes results in stunted growth, dark-green leaves and late-flowering.  We have also isolated the gai mutant gene (gai-1) from Arabidopsis. This mutant has a 17 amino acid deletion in the conserved DELLA domain of the GAI protein, which results in protein stabilization and extreme dwarfing in the mutant plants. We have generated transgenic petunia plants in which the gai mutant protein is over-expressed under the control of an alcohol-inducible promoter. This system permits induction of the dominant Arabidopsis gai mutant gene at a desired stage of plant development in petunia plants by simple application of alcohol.  The mutant protein is expected to repress GA signaling and thus retard plant growth.