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.

Auxinic herbicides are widely used for control of broadleaf weeds in cereal crops and turfgrass. These herbicides are structurally similar to the natural plant hormone auxin, and induce several of the same physiological and biochemical responses at low concentrations. After several decades of research to understand the auxin signal transduction pathway, the receptors for auxin binding and resultant biochemical and physiological responses have recently been discovered in plants.However, the precise mode of action for the auxinic herbicides is not completely understood despite their extensive use in agriculture for over six decades. Auxinic herbicide-resistant weed biotypes offer excellent model species for uncovering the mode of action as well as resistance to these compounds. Compared with other herbicide families, the incidence of resistance to auxinic herbicides is relatively low, with only 29 auxinic herbicide-resistant weed species discovered to date. The relatively low incidence of resistance to auxinic herbicides has been attributed to the presence of rare alleles imparting resistance in natural weed populations, the potential for fitness penalties due to mutations conferring resistance in weeds, and the complex mode of action of auxinic herbicides in sensitive dicot plants. This review discusses recent advances in the auxin signal transduction pathway and its relation to auxinic herbicide mode of action. Furthermore, comprehensive information about the genetics and inheritance of auxinic herbicide resistance and case studies examining mechanisms of resistance in auxinic herbicide-resistant broadleaf weed biotypes are provided. Within the context of recent findings pertaining to auxin biology and mechanisms of resistance to auxinic herbicides, agronomic implications of the evolution of resistance to these herbicides are discussed in light of new auxinic herbicide-resistant crops that will be commercialized in the near future.

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Exposure of soybean to dicamba can result in leaf malformation and sometimes yield loss, but it is unclear how yield components are affected by exposure to low quantities of this herbicide. The objectives were to characterize soybean injury and quantify changes in seed yield and yield components of soybean plants exposed to dicamba, and determine if seed yield loss can be estimated from visual injury ratings. Nine dicamba rates (0, 0.06, 0.23, 0.57, 1.1, 2.3, 4.5, 9.1, and 22.7 g ae ha−1) were applied at three growth stages (V2 – two trifoliates, V5-five trifoliates, or R2-full flowering soybean) to Beck's brand ‘342NRR’ soybean planted near Lafayette, IN, in 2009 and 2010 and near Fowler, IN, in 2009. Visually estimated soybean injury of 20% at the V2, V5, or R2 timing was 0.676 to 0.937 g ha−1dicamba at 14 d after treatment (DAT) and 0.359 to 1.37 g ha−1dicamba at 28 DAT. Seed yield was reduced by 5% from 0.042 to 0.528 g ha−1dicamba and a 10% reduction was caused by 0.169 to 1.1 g ha−1dicamba. The number of seeds m−2, pods m−2, reproductive nodes m−2, and nodes m−2were the most sensitive yield components. Path analysis indicated that dicamba reduced seeds m−2, pods m−2, reproductive nodes m−2, and nodes m−2which were the main causes of seed yield loss from dicamba exposure. The correlation of seed yield loss and visual soybean injury was significant (P < 0.0001) for both the V2 treatment timing (R2= 0.92) and the V5 and R2 treatment timings (R2= 0.91). Early-season injury rating of 8% at the V2 treatment and 2% at the V5 or R2 treatments caused 10% or more yield loss.