Effect of the growth retardant LAB 198 999, an acylcyclohexanedione compound, on epicotyl elongation and metabolism of gibberellins A1 and A 20 in cowpea.

The effect of LAB 198 999 [3,5-dioxo-4-butyryl-cyclohexane carboxylic acid ethyl ester; a new plant growth retardant which competitively inhibits 2-oxoglutarate-dependent gibberellin (GA) dioxygenases] on elongation and in-vivo [(3)H]GA1 and [(3)H]GA20 metabolism in cowpea (Vigna sinensis L. cv Blackeye pea No. 5) epicotyls has been investigated. Gibberellins and LAB 198 999 were injected into the epicotyl at 25-30 mm from the apex. In intact seedlings, epicotyl elongation was inhibited by LAB 198 999 (25 μg · epicotyl(-1)), and the inhibition was counteracted by GA1 but not by GA20. In contrast to intact seedlings, the inhibitor enhanced epicotyl elongation in de-bladed seedlings and expiants, in the latter case proportionally to the amount of inhibitor applied (up to 50 μg · epicotyl(-1)), but not in explants made from paclobutrazol-treated seedlings. The inhibitor also enhanced dramatically the elongation induced in paclobutrazol-treated expiants by GA1, but not by GA20. The promotive effect of LAB 198 999 was associated with increased contents of GA1 and GA8 in the growing region of the epicotyl, indicating a dependence on endogenous GAs. The effect of LAB 198999 decreased progressively with the age of the seedlings, probably as a consequence of a decreased level of GAs in the epicotyl. Gibberellin substrates and metabolites in the growing region of the epicotyl (upper 20 mm) were fractionated and identified tentatively by high-performance liquid chromatography and radiocounting using a homogeneous on-line radioactivity detector. The metabolism of [(3)H]GA1(t) (tentative) to [(3)H]GA8(t), and that of [(3)H]GA20(t) to [(3)H]GA1(t) and [(3)H]GA29(t) in the epicotyl were blocked by LAB 198 999, that of the former more efficiently than the latter. The results presented support the hypothesis that GA1 is the active GA controlling elongation of cowpea epicotyls. They also show that both the promotion of epicotyl elongation in explants and the enhancement of the effect of exogenous GA1 by LAB 198 999 are the result of the inhibitor blocking the in-vivo 2β-hydroxylation of GA1.