Non-Target-Site Resistance to Herbicides: Recent Developments

Abstract

Non-target-site resistance (NTSR) to herbicides in weeds can be conferred as a result of the alteration of one or more physiological processes, including herbicide absorption, translocation, sequestration, and metabolism. The mechanisms of NTSR are generally more complex to decipher than target-site resistance (TSR) and can impart cross-resistance to herbicides with different modes of action. Metabolism-based NTSR has been reported in many agriculturally important weeds, although reduced translocation and sequestration of herbicides has also been found in some weeds. This review focuses on summarizing the recent advances in our understanding of the physiological, biochemical, and molecular basis of NTSR mechanisms found in weed species. Further, the importance of examining the co-existence of TSR and NTSR for the same herbicide in the same weed species and influence of environmental conditions in the altering and selection of NTSR is also discussed. Knowledge of the prevalence of NTSR mechanisms and co-existing TSR and NTSR in weeds is crucial for designing sustainable weed management strategies to discourage the further evolution and selection of herbicide resistance in weeds.

Inheritance and Molecular Characterization of a Novel Mutated AHAS Gene Responsible for the Resistance of AHAS-Inhibiting Herbicides in Rapeseed (Brassica napus L.)

“…The TSR mechanism largely involves mutation(s) in the target site of the action of an herbicide, resulting in an insensitive or less sensitive target protein of the herbicide [19,36]. The NTSR is endowed by any mechanism not belonging to the TSR, which include reduced herbicide uptake/translocation, increased herbicide metabolism, decreased rate of herbicide activation and/or sequestration [37,38]. Our experimental results indicated the herbicide-resistance in rapeseed mutant line K5 is caused by the alteration of Per with Ser at position 182 in BnAHAS1, resulting in the less sensitive target protein BnAHAS1 of the herbicides.…”

“…Therefore, the herbicide-resistance of the mutant K5 belongs to the TSR. Whether TSR and NTSR mechanisms coexist in the mutant K5 is necessary to investigate in the future [37]. It is expected that the "omics" strategy (genomics, transcriptomics, proteomics or metabolomics) will play an important role to unravel the genetic base of NTSR in rapeseed [38].…”

Genetic variation associated with PPO-inhibiting herbicide tolerance in sorghum

“…Alternately, NTSR includes diverse mechanisms, including reduced herbicide uptake/translocation, increased herbicide detoxification, decreased herbicide activation rates, and herbicide sequestration [31]. Metabolism-based NTSR is associated with the herbicide detoxification due to the increased activity of enzyme complexes, including esterases, cytochrome P450s, glutathione S-transferase (GSTs), and UDP-glucosyl transferase [32]. Unlike TSR, metabolism-based NTSR is largely polygenic and confers resistance to herbicides with multiple modes of action [31].…”

Confirmation and Characterization of the First Case of Acetolactate Synthase (ALS)-Inhibitor—Resistant Wild Buckwheat (Polygonum convolvulus L.) in the United States

“…The coexistence of both target and non-target site resistance mechanisms such as altered ALS gene and enhanced metabolism of ALS-inhibitors in the same weed species has been reported [10,33,34]. Although altered ALS gene is known to confer a high level of resistance [28], enhanced metabolism also can bestow a high level of resistance in some weed species [10,35,36].…”