Genetic regulation of gibberellin deactivation in Pisum

The regulation of gibberellin (GA) deactivation was examined using the sin (slender) mutation in the garden pea (Pisum sativum L). This mutation blocks the deactivation of GA20, the precursor of the bioactive GA1. Firstly, crosses were made to combine sin with the GA biosynthesis mutations na, lh′ and le-3. The combination sin na produced a novel phenotype, with long ('slender') basal internodes and extremely short ('nana') upper internodes. In contrast, the double mutant sin lh′ was phenotypically dwarf. The mutation sin causes an accumulation of GA20 in maturing seeds, and this was unaffected by na, since the na mutation is not expressed in seeds. In contrast, lh′ seeds did not accumulate GA20, since lh′ 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 GA20 metabolism, namely, GA20 to GA29, and GA29 to GA29-catabolite. In the vegetative plant, on the other hand, sin blocked the step GA20 to GA29, but not GA29 to GA29-catabolite; the steps GA20 to GA81 and GA20 to GA1 were also not impaired in this mutant. It is clear that the effects of sin, like those of na, are strongly organ-specific. The presence of separate enzymes for the steps GA20 to GA29 and GA29 to GA29-catabolite was suggested by the observation that GA8 inhibited the latter step, but not the former, and by the inability of GA20 and GA29 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.