Synthetic auxin herbicides are designed to mimic indole-3-acetic acid (IAA), an integral plant hormone affecting cell growth, development, and tropism. In this review, we explore target site genes in the auxin signaling pathway including SCFTIR1/AFB, Aux/IAA, and ARFs that are confirmed or proposed mechanisms for weed resistance to synthetic auxin herbicides. Resistance to auxin herbicides by metabolism, either by enhanced cytochrome P450 detoxification or by loss of pro-herbicide activation, is a major non-target-site resistance pathway. We speculate about potential fitness costs of resistance due to effects of resistance-conferring mutations, provide insight into the role of polyploidy in synthetic auxin resistance evolution, and address the genetic resources available for weeds. This knowledge will be the key to unlock the long-standing questions as to which components of the auxin signaling pathway are most likely to have a role in resistance evolution. We propose that an ambitious research effort into synthetic auxin herbicide/target site interactions is needed to 1) explain why some synthetic auxin chemical families have activity on certain dicot plant families but not others and 2) fully elucidate target-site cross-resistance patterns among synthetic auxin chemical families to guide best practices for resistance management.

Herbicide-resistant weed management is one of the greatest agricultural challenges in crop production. Thus, the quick identification of herbicide-resistant weeds is extremely important for management. This study aimed to evaluate resistance to PSI-inhibiting herbicides (diquat) and physiological response to paraquat application in Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker; syn.: Erigeron sumatrensis Retz.]. The research was conducted with two C. sumatrensis biotypes, one susceptible and the other with multiple resistance to herbicides from five different modes of action (glyphosate, paraquat, diuron, saflufenacil, and 2,4-D). A dose–response assay was carried out to evaluate herbicide resistance to diquat in the paraquat-resistant C. sumatrensis biotype. The enzymatic activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX), hydrogen peroxide (H₂O₂) content, and chlorophyll a (Chl a) fluorescence were measured in both biotypes after paraquat (400 g ai ha⁻¹) application. The dose–response assay confirmed resistance of C. sumatrensis to diquat with resistance factor levels of 26-fold and 6-fold for LD₅₀ and GR₅₀ values, respectively, compared with the susceptible biotype. Accumulation of H₂O₂ occurred more rapidly in the paraquat-susceptible biotype than in the resistant one. Paraquat treatment caused an increase in SOD and APX activity in the susceptible biotype, but antioxidant enzyme activities were unaffected by paraquat in the resistant one at 5 h after application (HAA). Chl a fluorescence increased across the first 4 HAA in both resistant and susceptible biotypes. However, at 24 HAA, the resistant biotype showed a decline in fluorescence close to untreated plants, while the susceptible biotype died, confirming resistance to diquat in the paraquat-resistant C. sumatrensis biotype. The paraquat-resistant biotype does not induce antioxidative enzymes, as a possible mechanism of resistance to paraquat, but shows rapid recovery of photosynthesis and continuous growth when subjected to paraquat, while the paraquat-susceptible biotype does not survive.

In this work, we evaluated the short time-induced oxidative stress–mediated rapid metabolic and physiological responses of resistant and susceptible Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker; syn.: Erigeron sumatrensis Retz.] to 2,4-D herbicide. Under fixed conditions (25 C and 65 ± 5% relative humidity), we assayed injury symptoms, chlorophyll a fluorescence, and antioxidative systems of biotypes both resistant and susceptible to 2,4-D (1,005 g ae ha⁻¹). Under 15 versus 25 C temperatures and light and dark conditions, oxidative stress–mediated damage was assayed on plants that received 2,4-D herbicide applications. The injury symptoms observed in the 2,4-D–resistant biotype were rapid necrosis in leaves within 30 min, with the reestablishment of normal growth within 1 to 2 wk after 2,4-D treatment. The basal antioxidant enzyme activities of superoxide dismutase, catalase, and ascorbate peroxidase were greater in the resistant than in the susceptible biotype, although the activities of all enzymes generally did not differ between untreated and treated in the resistant biotype. The resistant biotype showed great reduction (at 1 and 4 h after application) in the photosynthetic electron transport chain performance index, while these metabolic changes were only detected after 4 h in the susceptible biotype. The resistant biotype recovered from the foliar damage 1 to 2 wk after 2,4-D application, while the susceptible biotype was controlled. The production of H₂O₂ was responsive to temperature and increased more rapidly in the 2,4-D–resistant biotype than in the susceptible one at both 15 and 25 C; however, there was a greater increase at 25 C in the resistant biotype. H₂O₂ production was not light dependent in 2,4-D–resistant C. sumatrensis, with increases even under dark conditions. The 2,4-D–resistant biotype showed rapid photosynthetic damage, possibly due to the rapid necrosis and leaf disruption, and increased H₂O₂ content compared with the susceptible biotype.

Repeated applications of herbicides at the labelled rates have often resulted in the selection and evolution of herbicide-resistant weeds capable of surviving the labelled and higher rates in subsequent generations. However, the evolutionary outcomes of recurrent herbicide selection at low rates are far less understood. In this study of a herbicide-susceptible population of Lolium perenne ssp. multiflorum, we assessed the potential for low glufosinate rates to select for reduced susceptibility to the herbicide, and cross-resistance to herbicides with other modes of action. Reduced susceptibility to glufosinate was detected in progeny in comparison with the parental population following three rounds of selection at low glufosinate rates. Differences were mainly observed at the 0.5X, 0.75X, and 1X rates. Comparing the parental susceptible population and progeny from the second and third selection cycle, the percentage of surviving plants increased to values of LD₅₀ (1.31 and 1.16, respectively) and LD₉₀ (1.36 and 1.26, respectively). When treated with three alternative herbicides (glyphosate, paraquat, and sethoxydim), no plants of either the parental or successive progeny populations survived treatment with 0.75X or higher rates of these herbicides. The results of this study provide clear evidence that reduced susceptibility to glufosinate can evolve in weed populations following repeated applications of glufosinate at low herbicide rates. However, the magnitude of increases in resistance levels over three generations of recurrent low-rate glufosinate selection observed is relatively low compared with higher levels of resistance observed in response to low-rate selection with other herbicides (three fold and more).