2,4-DICHLOROPHENOXYBUTYRIC ACID-RESISTANT MUTANTS OF ARABIDOPSIS HAVEDEFECTS IN GLYOXYSOMAL FATTY-ACID BETA-OXIDATION

It has been demonstrated previously that 2,4-dichlorophenoxybutyric ac id (2,4-DB) is metabolized to produce a herbicide, 2,4-D, by the actio n of peroxisomal fatty acid beta-oxidation in higher plants. To isolat e mutants that have defects in peroxisomal fatty acid beta-oxidation, we screened mutant lines of Arabidopsis seedlings for growth in the pr esence of toxic levels of 2,4-DB. Twelve of the mutants survived; of t hese, four required sucrose for postgerminative growth. This result su ggests that these mutants have defects in peroxisomal fatty acid beta- oxidation, because peroxisomal fatty acid beta-oxidation plays an impo rtant role in producing sucrose from storage lipids during germination . Genetic analysis revealed that these mutants can be classified as ca rrying alleles at three independent loci, which we designated ped1, pe d2, and ped3, respectively (where ped stands for peroxisome defective) . The ped1 mutant lacks the thiolase protein, an enzyme involved in fa tty acid beta-oxidation during germination and subsequent seedling gro wth, whereas the ped2 mutant has a defect in the intracellular transpo rt of thiolase from the cytosol to glyoxysomes. Etiolated cotyledons o f both ped1 and ped2 mutants have glyoxysomes with abnormal morphology .