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Enhanced mineralization of [U-14C]2,4-dichlorophenoxyacetic acid in soil from the rhizosphere of Trifolium pratense
- Shaw, L.J., Burns, R.G.
- Applied and environmental microbiology 2004 v.70 no.8 pp. 4766-4774
- soil bacteria, mineralization, 2,4-D, herbicide residues, rhizosphere, Trifolium pratense, Lolium perenne, biodegradation, forest soils, genes, nucleotide sequences, soil pollution
- Enhanced biodegradation in the rhizosphere has been reported for many organic xenobiotic compounds, although the mechanisms are not fully understood. The purpose of this study was to discover whether rhizosphere-enhanced biodegradation is due to selective enrichment of degraders through growth on compounds produced by rhizodeposition. We monitored the mineralization of [U-14C]2,4-dichlorophenoxyacetic acid (2,4-D) in rhizosphere soil with no history of herbicide application collected over a period of 0 to 116 days after sowing of Lolium perenne and Trifolium pratense. The relationships between the mineralization kinetics, the number of 2,4-D degraders, and the diversity of genes encoding 2,4-D/-ketoglutarate dioxygenase (tfdA) were investigated. The rhizosphere effect on [14C]2,4-D mineralization (50 microgram g-1) was shown to be plant species and plant age specific. In comparison with nonplanted soil, there were significant (P < 0.05) reductions in the lag phase and enhancements of the maximum mineralization rate for 25- and 60-day T. pratense soil but not for 116-day T. pratense rhizosphere soil or for L. perenne rhizosphere soil of any age. Numbers of 2,4-D degraders in planted and nonplanted soil were low (most probable number, <100 g-1) and were not related to plant species or age. Single-strand conformational polymorphism analysis showed that plant species had no impact on the diversity of alpha-Proteobacteria tfdA-like genes, although an impact of 2,4-D application was recorded. Our results indicate that enhanced mineralization in T. pratense rhizosphere soil is not due to enrichment of 2,4-D-degrading microorganisms by rhizodeposits. We suggest an alternative mechanism in which one or more components of the rhizodeposits induce the 2,4-D pathway.