PsbA gene over-expression and enhanced metabolism conferring resistance to atrazine in Commelina communis

Abstract

Commelina communis L. is a troublesome weed in agronomic fields and increasingly threatens the yield security of corn in north-eastern China. Previously, we found that a C. communis population (JL-1) has evolved resistance to atrazine. Although the potential genetic and enzymic differences contributing to atrazine resistance in this population have been investigated, the specific molecular mechanisms underlying C. communis resistance are still poorly understood. Here, the expression level of the target gene PsbA and the non-target-site resistance (NTSR) mechanism for this population were studied. The results showed that the decline in chlorophyll content in JL-1 leaves was less than in the susceptible JS-10 population following atrazine treatment. JL-1 exhibited an enhanced expression of the PsbA gene compared with JS-10 of 7.28- and 14.28-fold higher at 0 and 24 h after treatment with atrazine, respectively. The cytochrome P450 monooxygenase (P450) inhibitor piperonyl butoxide (PBO) increased the phytotoxicity of atrazine in both populations of C. communis. Seven candidate genes associated with NTSR of Jl-1 were identified through RNA-seq and validated by quantitative real-time PCR, including 5 upregulated genes involved in herbicide metabolism. In addition, the activities of glutathione S-transferases and P450s in JL-1 were increased compared with JS-10. Collectively, PsbA gene overexpression and enhanced metabolism are likely to be responsible for JL-1 resistance to atrazine.