Target-site mutation and enhanced metabolism endow resistance to nicosulfuron in a Digitaria sanguinalis population

• Published in: Pesticide biochemistry and physiology 2023-08, Vol.194, p.105488-105488, Article 105488
• Main Authors: Zhao, Bochui, Xu, Xian, Li, Binghua, Qi, Zhizun, Huang, Jinan, Hu, Ali, Wang, Guiqi, Liu, Xiaomin
• Format: Article
• Language: English
• Subjects: Acetolactate synthase; Acetolactate Synthase - metabolism; Digitaria - genetics; Digitaria sanguinalis; Enzyme Inhibitors - pharmacology; Glutathione S-transferases; Herbicide Resistance - genetics; Herbicides - pharmacology; Metabolic herbicide resistance; Mutation; Pyridines; Sulfonylurea Compounds - pharmacology; Target-site resistance
• ISSN: 0048-3575; 1095-9939
• DOI: 10.1016/j.pestbp.2023.105488

Digitaria sanguinalis is a competitive and annual grass weed that commonly infests crops across the world. In recent years, the control of D. sanguinalis by nicosulfuron has declined in Hebei Province, China. To determine the resistance mechanisms of D. sanguinalis to nicosulfuron, a population of D. sanguinalis where nicosulfuron had failed was collected from a maize field of Hebei Province, China. Whole-plant dose–response experiments demonstrated that the resistant population (HBMT-15) displayed 6.9-fold resistance to nicosulfuron compared with the susceptible population (HBMT-5). Addition of the glutathione S-transferase (GSTs) inhibitor 4-chloro-7-nitrobenzoxadiazole (NBD-Cl) significantly reduced the resistance level of the HBMT-15 population to nicosulfuron, and the GSTs activity of the HBMT-15 population was higher than the HBMT-5 population after nicosulfuron treatment. In vitro acetolactate synthase (ALS) enzyme experiments revealed that the nicosulfuron I50 value for the HBMT-15 population was 41 times higher than that of the HBMT-5 population. An Asp376 to Glu substitution in the ALS gene was identified in the HBMT-15 population. The HBMT-15 population had a moderate (2- to 4-fold) level of cross-resistance to three other ALS inhibitors (imazethapyr, pyroxsulam, and flucarbazone‑sodium), but was susceptible to pyrithiobac‑sodium. This study demonstrated that both an Asp376 to Glu substitution in the ALS gene and GSTs-involved metabolic resistance to ALS inhibitors coexisted in a D. sanguinalis population. [Display omitted] •Digitaria sanguinalis developed cross-resistance to ALS-inhibitors•GSTs inhibitor reversed nicosulfuron resistance in resistant D. sanguinalis•An Asp376Glu substitution was firstly identified in D. sanguinalis•Nicosulfuron treatment increased the activity of GSTs in resistant D. sanguinalis•Two resistance mechanisms were coexisted in resistant D. sanguinalis