SummaryThe regulation of gibberellin (GA} deactivation was examined using the sin (slander) mutation in the garden pea (Pisum sativum L.). This mutation blocks the deactivation of GA2o, the precursor of the bioactive GAl. Firstly, crosses were made to combine sin with the GA biosynthesis mutations na, Ih i and 1~3. The combination sin na produced a novel phenotype, with long ('slender') basel internodes and extremely short ('nana') upper internodes. In contrast, the double mutant sin Ih i was phenotypically dwarf. The mutation sin causes an accumulation of GAzo in maturing seeds, and this was unaffected by ha, since the na mutation is not expressed in seeds. In contrast, II1 i seeds did not accumulate GA20, since Ih i imposes an early block on GA biosynthesis. Secondly, the effects of sin on several steps in GA deactivation were investigated. In maturing seeds, the mutation sin blocks two steps in GA20 metabolism, namely, GA=0 to GA29, and GAS9 to GA2s-catabolite. In the vegetative plant, on the other hand, sin blocked the step GAS0 to GAz9, but not GAz9 to GAzscatabolite; the steps GA20 to GAS 1 and GAz0 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 GAz0 to GAzs and GA2s to GAzs-catabolite was suggested by the observation that GA s inhibited the latter step, but not the former, and by the inability of GAz0 and GAz9 to inhibIt each other's metabolism. It is suggested that the Sin gene may be a regulatory gene controlling the expression of two structural genes involved in GA deactivation.