Herbicides are the foundation of weed control in commercial crop-production systems. However, herbicide-resistant (HR) weed populations are evolving rapidly as a natural response to selection pressure imposed by modern agricultural management activities. Mitigating the evolution of herbicide resistance depends on reducing selection through diversification of weed control techniques, minimizing the spread of resistance genes and genotypes via pollen or propagule dispersal, and eliminating additions of weed seed to the soil seedbank. Effective deployment of such a multifaceted approach will require shifting from the current concept of basing weed management on single-year economic thresholds.

Increased EPSPS gene amplification and EPSPS enzyme activity confer resistance to glyphosate in the Des03 population. This is the first report of EPSPS gene amplification in glyphosate-resistant Italian ryegrass. Other resistance mechanism(s) may also be involved.

SummaryResistance occurs when a genetic change allows a population of weeds to survive a herbicide treatment to which the original population was susceptible. Individual plants of weed species that are resistant to a particular herbicide are typically present in untreated populations at very low frequencies. These few resistant individuals survive a herbicide application and reproduce, whereas susceptible individuals are killed and do not reproduce. The percentage of resistant individuals increases over time as the herbicide treatment is repeated. Weed scientists began identifying resistant weed biotypes (genotypes) about 40 years ago, and the number of weeds with resistant biotypes has increased in recent years. Use of a few modes of herbicide action in the major row crops, cotton (Gossypium hirsutum), corn (Zea mays), and soybean (Glycine max), has selected for resistance in certain weeds. Widespread use of the acetolactate synthase (ALS) inhibiting herbicides and glyphosate has led to resistance to one or both of these modes of action in weeds including Palmer amaranth (Amaranthus palmeri), common cocklebur (Xanthium strumarium), and horseweed (Conyza canadensis). Growers should diversify weed management tactics to avoid selecting more resistant weeds. Scout to detect uncontrolled weeds early and prevent movement of possibly resistant weed seed among fields. To reduce the rate of resistance buildup, practice rotation of all management factors where possible, including type of tillage, crops grown, and herbicide modes of action. Crop monoculture and continuous use of the same modes of action will accelerate resistance buildup and increase the difficulty and cost of weed control. What is Herbicide Resistance?Herbicide resistance is the inherited ability of a weed biotype to survive and reproduce despite exposure to a dose of herbicide that previously was effective on an unselected population. Application of a herbicide may reveal individuals within a population that already possess the capacity to survive exposure. Repeated, successive use of one herbicide, or herbicides with the same mode of action, increases the likelihood that resistant individuals will survive and reproduce. How are Weed Populations Selected for Resistance?The rate at which a resistant weed population is selected depends on the number and frequency of herbicide applications the population receives, the size of the population and its genetic diversity, and characteristics of the herbicide target site. Resistance buildup is accelerated when the management of crops does not include diverse tactics that limit herbicide use such as crop rotation and mechanical weed management. For example, there may be more opportunities for resistance buildup in conservation tillage because weeds are not killed by mechanical disturbance and non-selective herbicides such as glyphosate, paraquat, or glufosinate are used for pre-plant burndown. What are Herbicide Modes of Action?Mode of action describes the plant process affected by the herbicide that results in d...

Development of herbicide-resistant crops has resulted in significant changes to agronomic practices, one of which is the adoption of effective, simple, low-risk, crop-production systems with less dependency on tillage and lower energy requirements. Overall, the changes have had a positive environmental effect by reducing soil erosion, the fuel use for tillage, and the number of herbicides with groundwater advisories as well as a slight reduction in the overall environmental impact quotient of herbicide use. However, herbicides exert a high selection pressure on weed populations, and density and diversity of weed communities change over time in response to herbicides and other control practices imposed on them. Repeated and intensive use of herbicides with the same mechanisms of action (MOA; the mechanism in the plant that the herbicide detrimentally affects so that the plant succumbs to the herbicide; e.g., inhibition of an enzyme that is vital to plant growth or the inability of a plant to metabolize the herbicide before it has done damage) can rapidly select for shifts to tolerant, difficult-to-control weeds and the evolution of herbicide-resistant weeds, especially in the absence of the concurrent use of herbicides with different mechanisms of action or the use of mechanical or cultural practices or both.

Safeners are chemical agents that reduce the phytotoxicity of herbicides to crop plants by a physiological or molecular mechanism, without compromising weed control efficacy. Commercialized safeners are used for the protection of large-seeded grass crops, such as corn, grain sorghum, and wet-sown rice, against preplant-incorporated or preemergence-applied herbicides of the thiocarbamate and chloroacetanilide families. Safeners also have been developed to protect winter cereal crops such as wheat against postemergence applications of aryloxyphenoxypropionate and sulfonylurea herbicides. The use of safeners for the protection of corn and rice against sulfonylurea, imidazolinone, cyclohexanedione, isoxazole, and triketone herbicides also is well established. A safener-induced enhancement of herbicide detoxification in safened plants is widely accepted as the major mechanism involved in safener action. Safeners induce cofactors such as glutathione and herbicide-detoxifying enzymes such as glutathione S-transferases, cytochrome P450 monooxygenases, and glucosyl transferases. In addition, safeners enhance the vacuolar transport of glutathione or glucose conjugates of selected herbicides. The safener-mediated induction of herbicide-detoxifying enzymes appears to be part of a general stress response.