ABSCISIC-ACID IS A CAUSATIVE FACTOR IN THE MODE OF ACTION OF THE AUXINIC HERBICIDE QUINMERAC IN CLEAVER (GALIUM-APARINE L)

Hydroponic treatment of cleaver plants (Galium aparine L.) with the quinolinecarboxylic acid herbicide quinmerac caused early symptoms, which were elicited within 48 h of quinmerac application (10(-6) to 10(-5) mol . L(-1)) and characterized by stem and leaf epinasty, retardation of root and particularly shoot growth, and reduction in water consumption. The levels of 1-aminocyclopropane-1-carboxylic acid (ACC), ethylene and conjugated ACC began to increase within 3 h and peaked at 24 h, 48 h, and 72 h of treatment, respectively. HCN was increasingly released from Galium shoots into the gas phase after 2 to 3 days of quinmerac application. The concentrations of gibberellins, cytokinins, and 3-indoleacetic acid (IAA) were only slightly changed. Within 24 h of treatment, the respective abscisic acid (ABA) levels in the shoot tissue were elevated up to 20-fold, relative to the control. Application of 10(-4) mol . IL(-1) IAA increased ACC and ABA contents in Galium shoot and root tissues and induced phenotypic alterations in plants similar to those caused by quinmerac. Quinmerac-induced ABA accumulation was in close correlation with reductions in stomatal aperture, water consumption, photosynthetic CO2 uptake, and shoot and root fresh weights. Exogenously applied ABA mimicked quinmerac action on these parameters at comparable endogenous ABA concentrations. Additional treatment with the ACC synthesis inhibitor PACME decreased quinmerac-induced ACC formation, ABA accumulation, leaf epinasty and reduction of shoot growth. The effects of quinmerac could partly be restored when plants were additionally treated with ACC. This strongly suggests that ABA, induced ultimately through quinmerac-stimulated ACC synthesis, contributes to the auxinic mode of action underlying the inhibition of growth in cleaver.