2,4-Dichlorophenoxybutyric acid-resistant mutants of Arabidopsis have defects in glyoxysomal fatty acid beta-oxidation.
It has been demonstrated previously that 2,4-dichlorophenoxybutyric acid (2,4-DB) is metabolized to produce a herbicide, 2,4-D, by the action of peroxisomal fatty acid beta-oxidation in higher plants. To isolate mutants that have defects in peroxisomal fatty acid beta-oxidation, we screened mutant lines of Arabidopsis seedlings for growth in the presence of toxic levels of 2,4-DB. Twelve of the mutants survived; of these, four required sucrose for postgerminative growth. This result suggests that these mutants have defects in peroxisomal fatty acid beta-oxidation, because peroxisomal fatty acid beta-oxidation plays an important role in producing sucrose from storage lipids during germination. Genetic analysis revealed that these mutants can be classified as carrying alleles at three independent loci, which we designated ped1, ped2, and ped3, respectively (where ped stands for peroxisome defective). The ped1 mutant lacks the thiolase protein, an enzyme involved in fatty acid beta-oxidation during germination and subsequent seedling growth, whereas the ped2 mutant has a defect in the intracellular transport of thiolase from the cytosol to glyoxysomes. Etiolated cotyledons of both ped1 and ped2 mutants have glyoxysomes with abnormal morphology.[1]References
- 2,4-Dichlorophenoxybutyric acid-resistant mutants of Arabidopsis have defects in glyoxysomal fatty acid beta-oxidation. Hayashi, M., Toriyama, K., Kondo, M., Nishimura, M. Plant Cell (1998) [Pubmed]
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