Molecular Basis of Resistance to Bensulfuron-Methyl in a Smallflower Umbrella Sedge (Cyperus difformis L.) Population from China

Abstract

Smallflower umbrella sedge (Cyperus difformis L.) is an invasive weed, and infestations of C. difformis are increasing in rice (Oryza sativa L.) fields in China. Bensulfuron-methyl is a widely used sulfonylurea herbicide that inhibits the acetolactate synthase (ALS) enzyme and has been used in recent years for effectively controlling annual weeds in the Cyperaceae family. In this study, a suspected resistant population of C. difformis (BBHY1) was collected from a rice field in Huaiyuan County, Anhui Province, China, that survived treatment with bensulfuron-methyl at the field-recommended rate (FRR). Single-dose tests and whole-plant bioassays confirmed that the BBHY1 population was resistant to bensulfuron-methyl and had evolved a high level of resistance, with a resistance index (RI) of 12.87. Sequencing of the ALS gene revealed a CCT to CAT point mutation at codon 197, which caused a P-to-H substitution in the resistant plants. Analysis of the relative expression of ALS revealed no significant differences between the resistant and susceptible populations. Inhibiting the activity of cytochrome P450s (P450s) or glutathione S-transferases (GSTs) had no significant effect on bensulfuron-methyl resistance. The BBHY1 population exhibited cross-resistance to pyrazosulfuron-ethyl, penoxsulam, and bispyribac-sodium, with RIs ranging from 5.48 to 20.63, but remained susceptible to MCPA sodium, florpyrauxifen-benzyl, and bentazon, with RIs of <1.00. These herbicides could be potentially used as alternatives for controlling resistant populations and managing herbicide resistance in other aggressive weeds in rice fields.

Cytochrome P450s-Involved Enhanced Metabolism Contributes to the High Level of Nicosulfuron Resistance in Digitaria sanguinalis from China

“…According to local farmers, the field from which the R population was collected has been continually treated with ALS herbicides for more than 10 years. This suggests that the long-term use of a single herbicide inevitably facilitates resistance evolution [14].…”

“…For TSR, mutations in genes encoding the target proteins of a herbicide may be the main cause of ALS resistance, and it usually evolves cross-resistance to different herbicides with the same mode of action (MOA) [13]. To date, a total of nine codon positions in ALS have been reported [14,15]. Target-site mutations could confer a high level of resistance in D. sanguinalis [16].…”