ABSTRACT
The effect of the herbicide isoxaben on the incorporation of radiolabeled glucose, leucine, uracil, and acetate into acid insoluble cell wall material, protein, nucleic acids, and fatty acids, respectively, was measured. Dichlobenil, cycloheximide, actinomycin D, and cerulenin, inhibitors of the incorporation of these precursors into these macromolecular components, functioned as expected, providing positive controls. The incorporation of radiolabeled glucose into an acid insoluble cell wall fraction was severely inhibited by isoxaben at nanomolar concentrations. Amitrole, fluridone, ethalfluralin, and chlorsulfuron, as well as cycloheximide, actinomycin D, and cerulenin did not inhibit incorporation of glucose into this fraction, ruling out a general nonspecific effect of herbicides on glucose incorporation. The evidence thus suggests that isoxaben is an extremely powerful and specific inhibitor of cell wall biosynthesis.
ABSTRACT
An isoxaben resistant mutant of Arabidopsis thaliana is described whose locus, Ixr B1, is unlinked genetically to the previously described resistance locus Ixr A (DR Heim, JL Roberts, PD Pike, IM Larrinua [1989] Plant Physiol 90: 146-150). A cross of strains each homozygous for one of these two resistance loci gives rise to some isoxaben sensitive F(2) progeny. Growth curves versus isoxaben of this mutant, its F(1) progeny and the wild-type parent strain showed that this locus displays a weakly codominant Mendelian phenotype. Callus cultures were established from plants homozygous as well as heterozygous for this locus. Growth inhibition curves done with these cultures mimic the data obtained in vivo.
ABSTRACT
Interference with histidine metabolism, inhibition of pigment biosynthesis, or both have been the principal candidates for the primary site of action of 3-amino 1,2,4-triazole (amitrole). Arabidopsis thaliana is sensitive to 1,2,4-triazole-3-alanine, a feedback inhibitor of histidine biosynthesis, and this effect is reversed by histidine. The combination of triazolealanine and histidine, however, does not reverse the herbicidal effect of amitrole. This indicates that amitrole toxicity is not caused by histidine starvation, nor is it caused by the accumulation of a toxic intermediate of the histidine pathway. Amitrole inhibits root elongation at lower concentrations than it causes pigment bleaching in the leaves. In contrast, fluridone, a known inhibitor of the carotenoid biosynthetic pathway does not block root elongation. Fluridone also inhibits carotenoid accumulation in etiolated seedlings in the dark, but amitrole does not. Last, gabaculine and acifluorfen, but not amitrole, prevent chlorophyll accumulation in greening etiolated seedlings of Arabidopsis. These experiments cast doubt on pigment biosynthesis as the primary site of action of amitrole.
ABSTRACT
Mutants resistant to the herbicide N-(3-[1-ethyl-1-methylpropyl]-5-isoxazolyl)-2,6,dimethoxybenzamide (isoxaben) were recovered from an M2 population of Arabidopsis thaliana. Two of these mutants, DH47 and DH48, had a high level of resistance in the homozygous state. Crosses of these mutants to marker strains, and to each other, showed that each contained a mutation at a single locus tightly linked to lutescens, a marker on the fifth chromosome of A. thaliana. Growth curves of these mutants and of the F1 progeny of a cross with the wild type parent strain, in the presence of different concentrations of the herbicide, showed that both mutants display a semidominant phenotype. The two mutations differed in their degree of resistance, both as homozygotes and heterozygotes. This suggests that they are two different alleles. Callus cultures were established from plants homozygous, as well as heterozygous, for each of these mutations. Growth curves of these cultures in the presence of the herbicide mimicked the data obtained in vivo indicating that sensitivity to isoxaben is not dependent on a differentiated function.
