Metabolic resistance to acetolactate synthase (ALS)-inhibiting herbicide tribenuron-methyl in Descurainia sophia L. mediated by cytochrome P450 enzymes
D. sophia is one of the most notorious broadleaf weed in China, and has evolved extremely high resistance to ALS-inhibiting herbicide tribenuron-methyl. The target-site resistance due to ALS gene mutations was known well, while the non-target-site resistance is not yet well-characterized. Metabolic resistance, which is conferred by enhanced rates of herbicide metabolism, is the most important NTSR. To explore the mechanism of metabolic resistance underlying resistant (R) D. sophia plants, tribenuron-methyl uptake and metabolism levels, qPCR reference gene stability, and candidate P450 genes expression patterns were investigated. The results of liquid chromatography-mass spectrometry (LC-MS) analysis indicated that the metabolic rates of tribenuron-methyl in R plants was significantly faster than in susceptible (S) plants, and this metabolism differences can be eliminated by P450 inhibitor malathion. 18S rRNA and TIP41-like were identified as the most suitable reference genes using programs of BestKeeper, NormFinder and geNorm. The P450 gene CYP96A146 constitutively overexpressed in R plants compared to S plants, this overexpression in R plants can be suppressed by malathion. Taken together, higher expression level of P450 genes, leading to higher tribenuron-methyl metabolism, appears to be responsible for metabolic resistance to tribenuron-methyl in R D. sophia plants.