Non-target-site and target-site resistance to AHAS inhibitors in American sloughgrass (Beckmannia syzigachne)

• Published in: Journal of Integrative Agriculture Vol. 17; no. 12; pp. 2714 - 2723
• Main Authors: WANG, Jing-jing, LI, Xiang-ju, LI, Dan, HAN, Yu-jiao, LI, Zheng, YU, Hui-lin, CUI, Hai-lan
• Format: Journal Article
• Language: English
• Published: Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, P.R.China 01.12.2018; Elsevier
• Subjects: American sloughgrass; cross-resistance; gene mutation; non-target-site resistance; American sloughgrass; cross-resistance; gene mutation; non-target-site resistance
• ISSN: 2095-3119
• DOI: 10.1016/S2095-3119(18)62021-0

American sloughgrass (Beckmannia syzigachne (Steud.) Fernald) is one of the most competitive and malignant weeds in rice-wheat rotation fields in China. American sloughgrass populations in the Jiangsu Province of China became less sensitive to acetohydroxyacid synthase (AHAS) inhibitors after repeated application for many years in these areas. Two suspected resistant American sloughgrass populations (R1 and R2) collected in the field were detected the resistance to inhibitors of AHAS in whole-plant dose-response assays, compared to the susceptible (S) population. These assays indicated that R1 showed low resistance to mesosulfuron-methyl (3.32-fold), imazapic (2.84-fold) and pyroxsulam (1.55-fold), moderate resistance to flazasulfuron (4.67-fold) and pyribenzoxim (7.41-fold), and high resistance to flucarbazone (11.73-fold). However, using a combination of the cytochrome P450 inhibitor, malathion, with mesosulfuron-methyl resulted in a reduction in R1 resistance relative to mesosulfuron-methyl alone. Furthermore, R2 was highly resistant to flazasulfuron (34.90-fold), imazapic (11.30-fold), flucarbazone (49.20-fold), pyribenzoxim (12.94-fold), moderately resistant to mesosulfuron-methyl (9.77-fold) and pyroxsulam (6.26-fold), and malathion had no effect on R2 resistance to mesosulfuron-methyl. The full-length of AHAS genes was sequenced and the AHAS enzymes were assayed in vitro in order to clarify the mechanism of resistance to AHAS inhibitors in R1 and R2 populations. The results demonstrated that R2 had a Pro-197-Ser mutation in the AHAS gene, and the sensitivity of R2 to the five AHAS inhibitors was decreased, which may result in R2 resistance to AHAS inhibitors. There was no mutation in the AHAS gene of R1, and there were no significant differences in enzyme sensitivity between susceptible (S) and resistant (R1) populations. An enhanced metabolism may be the main mechanism of R1 resistance to AHAS inhibitors.