The widely successful use of synthetic herbicides over the past 70 years has imposed strong and widespread selection pressure, leading to the evolution of herbicide resistance in hundreds of weed species. Both target-site resistance (TSR) and non-target-site resistance (NTSR) mechanisms have evolved to most herbicide classes. TSR often involves mutations in genes encoding the protein targets of herbicides, affecting the binding of the herbicide either at or near catalytic domains or in regions affecting access to them. Most of these mutations are non-synonymous single-nucleotide polymorphisms, but polymorphisms in more than one codon or entire codon deletions have also evolved. Some herbicides bind multiple proteins, making TSR mechanisms more difficult to evolve. Increased amounts of protein target, by increased gene expression or by gene duplication, is an important, albeit less common, TSR mechanism. NTSR mechanisms include reduced absorption or translocation and increased sequestration or metabolic degradation. The mechanisms that can contribute to NTSR are complex and often involve genes that are members of large gene families. For example, enzymes involved in herbicide metabolism-based resistances include cytochromes P450, glutathione-S-transferases, glucosyl and other transferases, aryl acylamidase, and others. Both TSR and NTSR mechanisms can combine at the individual level to produce higher resistance levels. The vast array of herbicide-resistance mechanisms for generalist (NTSR) and specialist (TSR and some NTSR) adaptations that have evolved over a few decades illustrate the evolutionary resilience of weed populations to extreme selection pressures. These evolutionary processes drive herbicide and herbicide-resistant crop development and resistance management strategies.
Keywords: evolution; herbicide; mutant; plant biochemistry; plant defense; plant molecular biology; plant physiology; resistance mechanism; xenobiotic.
Published under license by The American Society for Biochemistry and Molecular Biology, Inc.
Non-Target-Site Resistance to Herbicides: Recent Developments.Plants (Basel). 2019 Oct 15;8(10):417. doi: 10.3390/plants8100417. Plants (Basel). 2019. PMID: 31618956 Free PMC article. Review.
ALOMYbase, a resource to investigate non-target-site-based resistance to herbicides inhibiting acetolactate-synthase (ALS) in the major grass weed Alopecurus myosuroides (black-grass).BMC Genomics. 2015 Aug 12;16(1):590. doi: 10.1186/s12864-015-1804-x. BMC Genomics. 2015. PMID: 26265378 Free PMC article.
Unravelling the genetic bases of non-target-site-based resistance (NTSR) to herbicides: a major challenge for weed science in the forthcoming decade.Pest Manag Sci. 2013 Feb;69(2):176-87. doi: 10.1002/ps.3318. Epub 2012 May 21. Pest Manag Sci. 2013. PMID: 22614948
Transcriptional markers enable identification of rye-grass (Lolium sp.) plants with non-target-site-based resistance to herbicides inhibiting acetolactate-synthase.Plant Sci. 2017 Apr;257:22-36. doi: 10.1016/j.plantsci.2017.01.009. Epub 2017 Jan 20. Plant Sci. 2017. PMID: 28224916
Evolution in action: plants resistant to herbicides.Annu Rev Plant Biol. 2010;61:317-47. doi: 10.1146/annurev-arplant-042809-112119. Annu Rev Plant Biol. 2010. PMID: 20192743 Review.