Changes in gibberellin levels in the flowering shoot ofPhalaenopsis hybrida under high temperature conditionswhen flower development is blocked

Abstract The ability of exogenous gibberellin (GA) A 3 to substitute for low temperatures in inducing flowering in Phalaenopsis hybrida under high temperatures suggests a similar role for endogenous GAs in normal (low temperature) development of the inflorescence and floral buds. Changes in endogenous GAs in shoot-tips (about 2.0 cm long) were examined when the potentially flowering shoot was 2–3 cm and 7–10 cm long, respectively. Treatments included warm control (30/25 °C day/night, non-flowering), GA 3 -treated (30/25 °C day/night, flowering) and cool-induced (25/20 °C day/night, flowering) plants. GA 3 at 0.5 μg·shoot –1 was injected into the cavity of the second visible bud scale below the flowering shoot apex. The contents in the tips of potentially flowering shoots of GA 1 , GA 20 , GA 19 and GA 53 tended to be highest in cool-induced plants, intermediate in GA 3 -treated plants, and lowest in the warm controls (non-flowering). Tips of potentially flowering shoots in warm controls also contained higher GA 8 relative to GA 3 -treated and cool-induced plants. Tips of potentially flowering shoots (2–3 cm in length with no flower primordium), contained low levels of GAs than older 7–10 cm long flowering shoots (with flower primordia) under cool-inductive conditions. These results suggest that continued inflorescence development and flower bud initiation are closely associated with increases in endogenous GAs, even in GA 3 -treated plants. They also suggest that a more rapid biosynthetic flow-through from GA 19 →GA 20 →GA 1 →GA 8 leaving reduced levels of GA 1 may be involved in the inhibition of flowering and shoot elongation seen in warm (30/25 °C day/night) control plants. A reduced conversion of ‘active’ GA 1 to inactive GA 8 may thus be required for successful floral induction and development whether induced by cool temperatures or by applied GA 3 . These results imply that the high temperature inhibitory effect on flowering is mediated through its effect on lowering the level of endogenous GA 1 and its precursors.