Abstract
Abscisic acid (ABA) was shown to reduce the photosynthetic capacity of a leaf through an apparent inhibition of ribulose 1,5-bisphosphate (RuBP) carboxylase (RuBPCase) activity, in addition to promoting stomatal closure. By comparison with the effects of other inhibitors of photosynthesis (cyanazine, methyl viologen, sodium azide, nigericin, sodium cyanide) on whole leaf photosynthesis, RuBPCase activity and metabolite pool sizes, it was demonstrated that the biochemical basis for the apparent effect of ABA on RuBPCase activity was not the result of reduced substrate availability, decarbamylation of the enzyme, or synthesis of carboxyarabinitol 1-phosphate, the naturally occurring tight-binding inhibitor of the enzyme. An inhibition of photosynthetic capacity showing the same biochemical characteristics as ABA-fed leaves was observed in plants grown under saline conditions. We suggest that the common link between environmental stress and reductions in photosynthetic capacity may be ABA. We hypothesize that ABA may affect plasma membrane function and thus indirectly RuBPCase activity through altered ion fluxes. The results of feeding cyanazine, methyl viologen, and nigericin provide additional evidence that regulation of RuBPCase activity by carbamylation/decarbamylation is related to the extent to which the capacity for ATP formation limits photosynthesis.