Genetic regulation of gibberellin deactivation in Pisum

Summary 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 GA 20 , the precursor of the bioactive GA 1 . Firstly, crosses were made to combine sin with the GA biosynthesis mutations na , lh i 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 i was phenotypically dwarf. The mutation sin 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 sin on several steps in GA deactivation were investigated. In maturing seeds, the mutation sin 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, sin 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 sin , 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 Sin gene may be a regulatory gene controlling the expression of two structural genes involved in GA deactivation.