Descurainia sophia L. (flixweeds) is a noxious broad-leaf weed infesting winter wheat fields in China that has evolved high resistance to tribenuron-methyl. In this work, a brand new gene CYP77B34 was cloned from tribenuron-methyl-resistant (TR) D. sophia and transferred into Arabidopsis thaliana, and the sensitivities of Arabidopsis with or without the CYP77B34 transgene to herbicides with a different mode of actions (MoAs) were tested. Compared to Arabidopsis expressing pCAMBIA1302-GFP (empty plasmid), Arabidopsis transferring pCAMBIA1302-CYP77B34 (recombinant plasmid) became resistant to acetolactate synthase (ALS)-inhibiting herbicide tribenuron-methyl, protoporphyrinogen oxidase (PPO)-inhibiting herbicides carfentrazone-ethyl and oxyfluorfen. Cytochrome P450 inhibitor malathion could reverse the resistance to tribenuron-methyl, carfentrazone-ethyl and oxyfluorfen in transgenic Arabidopsis plants. In addition, the metabolic rates of tribenuron-methyl in Arabidopsis expressing CYP77B34 were significantly higher than those in Arabidopsis expressing pCAMBIA1302-GFP. Other than that, the transgenic plants showed some tolerance to very-long-chain fatty acid synthesis (VLCFAs)-inhibiting herbicide pretilachlor and photosystem (PS) II-inhibiting herbicide bromoxynil. Subcellular localization revealed that the CYP77B34 protein was located in the endoplasmic reticulum (ER). These results clearly indicated that CYP77B34 mediated D. sophia resistance to tribenuron-methyl and may have been involved in D. sophia cross-resistance to carfentrazone-ethyl, oxyfluorfen, pretilachlor and bromoxynil.

A population of Echinochloa crus-galli (L.) P. Beauv obtained from direct-seeding rice fields in Jiangxi Province, China, exhibited high resistance levels (13.5-fold) to the acetyl-CoA carboxylase (ACCase)-inhibiting herbicide cyhalofop-butyl. Compared with the susceptible (S) population, this resistant (R) population evolved a cross-resistance to aryloxyphenoxypropionates (APPs) herbicides metamifop (2.9-fold) and fenoxapro-p-ethyl (4.1-fold), cyclohexanediones (CHDs) herbicide clethodim (4.7-fold), phenyl pyrazoline (DEN) herbicide pinoxaden (6.4-fold), and evolved multiple-resistance to acetolactate synthase (ALS)-inhibiting herbicide penoxsulam (3.6-fold), and auxin mimic herbicides quinclorac (>34.7-fold) and florpyrauxifen-benzyl (2.4-fold). ACCase gene sequencing did not reveal the existence of any known mutation point conferring with herbicide resistance. In addition, three metabolic inhibitors—one glutathione—S-transferase (GST) inhibitor (NBD-Cl), and two cytochrome P450 inhibitors (malathion and PBO)—did not reverse the cyhalofop-butyl resistance. Furthermore, enhanced metabolic rates of more than 60% 24 h after treatment with the active compound cyhalofop acid was observed in R plants compared to S plants. Hence, enhanced metabolism activity endows a non-target-site resistance to cyhalofop-butyl in the R population of E. crus-galli. Future research will be required to determine what metabolizing enzyme genes are responsible for cyhalofop-butyl resistance in E. crus-galli.