GENETIC-REGULATION OF GIBBERELLIN DEACTIVATION IN PISUM

The regulation of gibberellin (GA) deactivation was examined using the sln (slender) mutation in the garden pea (Pisum sativum L.). This mutation blocks the deactivation of GA(20), the precursor of the bioactive GA(1). Firstly, crosses were made to combine sln with the GA biosynthesis mutations na, lh(i) and le-3. The combination sln na produced a novel phenotype, with long ('slender') basal internodes and extremely short ('nana') upper internodes. In contrast, the double mutant sln lh(i) was phenotypically dwarf. The mutation sln causes an accumulation of GA(20) in maturing seeds, and this was unaffected by na, since the na mutation is not expressed in seeds. In contrast, lh(i) seeds did not accumulate GA(20), since lh(i) imposes an early block on GA biosynthesis. Secondly, the effects of sln on several steps in GA deactivation were investigated. In maturing seeds, the mutation sln blocks two steps in GA(20) metabolism, namely, GA(20) to GA(29), and GA(29) to GA(29)-catabolite. In the vegetative plant, on the other hand, sln blocked the step GA(20) to GA(29), but not GA(29) to GA(29)-catabolite; the steps GA(20) to GA(81) and GA(20) to GA(1) were also not impaired in this mutant. It is clear that the effects of sln, like those of na, are strongly organ-specific. The presence of separate enzymes for the steps GA(20) to GA(29) and GA(29) to GA(29)-catabolite was suggested by the observation that GA(8) inhibited the latter step, but not the former, and by the inability of GA(20) and GA(29) to inhibit each other's metabolism. It is suggested that the Sln gene may be a regulatory gene controlling the expression of two structural genes involved in GA deactivation.