Pesticide degradation studies in soil are often performed at higher concentrations than can bemeasured in soils after conventional agriculture use. Therefore, biodegradation ratesdetermined for higher concentrations cannot be extrapolated to lower concentrations, whichmay explain residual concentration of pesticides even a long time after application.The purpose of the present study was i) to compare the half-life time of MCPAthroughout a mechanistic model based on the 14C-respiration rate at low and highconcentrations, and ii) to clarify if energy limitation and concentration thresholdscontrol the expression of functional genes involved in pesticide degradation, iii)to assess if the absence of functional gene expression is a possible mechanismsthat might explain the build-up of persistent pesticides and metabolite pools insoils. To test our assumption, we set up an incubation experiment for 4 weeks. 50 g topsoilsamples of a Luvisol from an agriculture field, were weighed into microcosms. Subsequently,the soil moisture was adjusted to a volumetric water content of 25 % with 14C-ring labelledMCPA solutions ranging from low (30-500 μg kg−1 soil) to high concentrations (1000-20000μg kg−1 soil). In the first degradation step, 2-methyl-4-chloro-phenoxyacetic acid (MCPA) isconverted to 4-chloro-2-methylphenol. The responsible α-ketoglutarate-dependentdioxygenase is encoded by the tfdA gene. To quantify the abundance of putative MCPAdegraders and their degradation potential, tfdA gene (DNA) and transcript (mRNA)abundances were estimated for each concentration through quantitative real-time PCR.Mineralization dynamics for each treatment were analyzed, following the release of14C-CO2 during microbial respiration. In addition, we quantified the assimilation ofMCPA-derived C by soil microorganism through 14C in microbial biomass C atthree distinct phases: lag, exponential increase and saturation phase, depending oncumulated 14C mineralization. The remaining model compound in the soil wereanalyzed using a combination of liquid chromatography (LC) and mass spectrometry(MS/MS). First results showed that tfdA gene expression depended on the added MCPAconcentrations. With increasing MCPA concentration the cDNA abundance increased up to alevel of 2⋅104 copies g−1 dry weight for the highest concentration. Low MCPAconcentrations (<1000 μg kg−1 soil) did not induce any detectable expression of tfdA genes.We suggest that the mechanisms of MCPA degradation depended on the initial MCPAconcentration: Whereas co-metabolisms might be the dominant pathway under lowMCPA concentrations, metabolic mineralization occurred at high concentrationswhich were visible from cumulative 14C-CO2respiration curves in sigmoidal forms. [ABSTRACT FROM AUTHOR]