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Herbicide options for selective control of monocot weeds in rice (Oryza sativa L.) have historically been limited to a few modes of action such as inhibitors of acetolactate synthase (e.g., penoxsulam, imazamox), photosystem II (e.g., propanil), and acetyl-CoA carboxylase (e.g., cyhalofop). Florpyrauxifen-benzyl (Rinskor™) is a synthetic auxin molecule introduced to the U.S. rice herbicide market in 2018, providing broad-spectrum weed control (monocots and dicots), including hard-to-control species such as barnyardgrass [Echinochloa crus-galli (L.) P. Beauv.], along with postemergence rice selectivity at very low use rates. Within the year of commercialization, field agronomists and academics identified E. crus-galli escapes in some areas where florpyrauxifen-benzyl had been sprayed. Further evaluation under controlled environments confirmed that those plants were able to survive florpyrauxifen-benzyl application at the label rate. Here, we identify the mechanism of resistance to florpyrauxifen-benzyl and penoxsulam in two E. crus-galli populations from Arkansas (AR-27) and Missouri (MO-18). Using high-resolution mass spectrometry, we compared the two resistant biotypes with known susceptible plants regarding their ability to metabolize florpyrauxifen-benzyl, florpyrauxifen-acid, and penoxsulam in planta. We discovered that the resistant plants share a common resistance mechanism to florpyrauxifen-benzyl and penoxsulam, involving hydrolysis of a methoxy group (likely mediated by a cytochrome P450 monooxygenase) followed by glucose conjugation. Given that penoxsulam has been widely used in rice fields for the past decade, these data suggest that some populations of E. crus-galli may have evolved resistance before the commercialization of florpyrauxifen-benzyl.

The mitotic-inhibiting herbicide pronamide controls susceptible annual bluegrass (Poa annua L.) pre- and postemergence, but in some resistant populations, postemergence activity is compromised, hypothetically due to a target-site mutation, lack of root uptake, or an unknown resistance mechanism. Three suspected pronamide-resistant (LH-R, SC-R, and SL-R) and two pronamide-susceptible (BS-S and HH-S) populations were collected from Mississippi golf courses. Dose–response experiments were conducted to confirm and quantify pronamide resistance, as well as resistance to flazasulfuron and simazine. Target sites known to confer resistance to mitotic-inhibiting herbicides were sequenced, as were target sites for herbicides inhibiting acetolactate synthase (ALS) and photosystem II (PSII). Pronamide absorption and translocation were investigated following foliar and soil applications. Dose–response experiments confirmed pronamide resistance of LH-R, SC-R, and SL-R populations, as well as instances of multiple resistance to ALS- and PSII-inhibiting herbicides. Sequencing of the α-tubulin gene confirmed the presence of a mutation that substituted isoleucine for threonine at position 239 (Thr-239-Ile) in LH-R, SC-R, SL-R, and BS-S populations. Foliar application experiments failed to identify differences in pronamide absorption and translocation between the five populations, regardless of harvest time. All populations had limited basipetal translocation—only 3% to 13% of the absorbed pronamide—across harvest times. Soil application experiments revealed that pronamide translocation was similar between SC-R, SL-R, and both susceptible populations across harvest times. The LH-R population translocated less soil-applied pronamide than susceptible populations at 24, 72, and 168 h after treatment, suggesting that reduced acropetal translocation may contribute to pronamide resistance. This study reports three new pronamide-resistant populations, two of which are resistant to two modes of action (MOAs), and one of which is resistant to three MOAs. Results suggest that both target site– and translocation-based mechanisms may be associated with pronamide resistance. Further research is needed to confirm the link between pronamide resistance and the Thr-239-Ile mutation of the α-tubulin gene.

The genetic and molecular basis of resistance evolution in weeds to multiple herbicides remains unclear despite being a great threat to agriculture. A population of late watergrass [Echinochloa phyllopogon (Stapf.) Koso-Pol.] was reported to exhibit resistance to ≥15 herbicides from six sites of action, including thiobencarb (TB). While previous studies disclosed that the resistance to a majority of herbicides such as acetolactate synthase (ALS) and acetyl-CoA carboxylase inhibitors is caused by the overexpression of herbicide-metabolizing cytochrome P450s (CYP81A12 and CYP81A21), the resistance mechanisms to some herbicides remain unknown. Here, we analyzed the resistance segregation in the progenies between resistant and sensitive populations and performed a transgenic plant sensitivity assay to resolve whether TB resistance is endowed by the same CYP81A12/21-based cross-resistance mechanism or other unknown multiple-resistance mechanisms. In the F6 progenies, resistance to the ALS inhibitor bensulfuron-methyl cosegregated with the resistances to many other herbicides under the CYP81A12/21-based cross-resistance mechanism; however, TB resistance segregated independently. Furthermore, CYP81A12/21 failed to confer TB resistance in transgenic Arabidopsis thaliana L. Heynh, thus confirming that TB resistance in resistant E. phyllopogon is not endowed by the two P450s that are responsible for the metabolism-based cross-resistance. This study provides evidence that resistance in E. phyllopogon to herbicides with multiple sites of action is endowed by both P450-based and other uncharacterized non–target site based mechanisms. Our findings add another layer in the understanding of resistance evolution to multiple herbicides in E. phyllopogon. Identification of the key genes endowing TB resistance will be the future direction of this research.

Herbicide-resistant weeds pose a severe threat to sustainable vegetation management in various production systems worldwide. The majority of the herbicide resistance cases reported thus far originate from agronomic production systems where herbicide use is intensive, especially in industrialized countries. Another notable sector with heavy reliance on herbicides for weed control is managed turfgrass systems, particularly golf courses and athletic fields. Intensive use of herbicides, coupled with a lack of tillage and other mechanical tools that are options in agronomic systems, increases the risk of herbicide-resistant weeds evolving in managed turfgrass systems. Among the notable weed species at high risk for evolving resistance under managed turf systems in the United States are annual bluegrass, goosegrass, and crabgrasses. The evolution and spread of multiple herbicide resistance, an emerging threat facing the turfgrass industry, should be addressed with the use of diversified management tools. Target-site resistance has been reported commonly as a mechanism of resistance for many herbicide groups, though non–target site resistance is an emerging concern. Despite the anecdotal evidence of the mounting weed resistance issues in managed turf systems, the lack of systematic and periodic surveys at regional and national scales means that confirmed reports are very limited and sparse. Furthermore, currently available information is widely scattered in the literature. This review provides a concise summary of the current status of herbicide-resistant weeds in managed turfgrass systems in the United States and highlights key emerging threats. Nomenclature: Annual bluegrass, Poa annua L.; crabgrass, Digitaria spp.; goosegrass, Eleusine indica (L.) Gaertn

The full spectrum of herbicide resistance in a weed can vary according to the mechanistic basis and cannot be implied from the selective pressure. Common ragweed (Ambrosia artemisiifolia L.) is an important weed species of horticultural crops that has developed resistance to linuron based on either target site– or non–target site resistance mechanisms. The objective of the study is to characterize the cross-resistance to metribuzin of linuron-selected biotypes of A. artemisiifolia with target site– and non–target site resistance and determine its genetic basis. Crosses were made between two types of linuron-resistant biotype and a linuron-susceptible biotype, and the progeny were further backcrossed with susceptible plants to the third backcross (BC3) generation to determine their responses to both herbicides compared with parental lines. The target site–based linuron-resistant biotype was cross-resistant to metribuzin, and resistance to both herbicides was maintained at the same level in the BC3 line. In contrast, the linuron-selected biotype with a non–target site resistance mechanism was not cross-resistant to metribuzin. In addition, the BC3 lines deriving from the non–target site resistant parents had very low-level resistance. While the target site–resistance trait is maintained through multiple crosses, non–target site based resistance would be lost over time when selection is absent or insufficient to retain all genes involved in resistance as a complex trait. This would imply A. artemisiifolia biotypes with different mechanisms would need to be managed differently over time.

Resistance to 2‐methyl‐4‐chloro‐phenoxyacetic acid (MCPA) was recently confirmed in a population of green pigweed (Amaranthus powellii) from Dresden, Ontario, Canada, with a resistance factor of 4.4. Resistance to synthetic auxin herbicides in Amaranthus species has previously been linked to non‐target site resistance mechanisms with low‐level resistance factors (< 10). Based on this information, an investigation into the mechanism of resistance to MCPA was conducted in this population of green pigweed. No significant differences in absorption, translocation, and metabolism of 14C‐MCPA existed between the resistant and a susceptible population of green pigweed. An RNA‐Sequencing experiment to identify differentially expressed genes also confirmed this result. Genes that were differentially expressed in the resistant population were linked to target site modifications. A single nucleotide polymorphism (SNP) conferring a leucine to phenylalanine substitution was identified in auxin response factor (ARF) 9. This mutation may be in the Phox and Bem1p (PB1) domain in ARF9, which facilitates the interaction between ARFs and Aux/IAA repressor proteins. The results demonstrate that the mechanism of resistance to MCPA is not a non‐target site mechanism and may be linked to a target site modification. Specifically, a SNP in ARF9 could disrupt the interaction between ARF9 and other Aux/IAAs, which could prevent ubiquitination of Aux/IAAs and subsequent lethal action of MCPA.

Silky windgrass is a serious weed in central and northern Europe. Its importance has escalated in recent years because of its growing resistance to acetolactate synthase (ALS)-inhibiting herbicides. This study investigated the resistance level for three herbicide sites of action in eight silky windgrass populations, collected in fields neighboring a field where iodosulfuron sodium salt–resistant silky windgrass had previously been found. Target site resistance (TSR) and non–target site resistance (NTSR) mechanisms were identified, and a spatial gradient distribution hypothesis of ALS resistance was tested. Populations showed large variations in ED50 values to iodosulfuron, with resistance indices (RIs) ranging from 0.1 to 372. No cross-resistance was found to other herbicide groups with the same site of action as iodosulfuron. In contrast, resistance was observed to the acetyl-CoA carboxylase inhibitor, fenoxaprop ethyl ester (RI from 0.7 to 776), while the activity of prosulfocarb, an inhibitor of long-chain fatty-acid synthesis, was unaffected. Iodosulfuron-resistant phenotypes were associated with NTSR, while fenoxaprop ethyl ester resistance was caused by both NTSR and TSR (Ile-1781-Leu mutation). A large-scale trend in the spatial distribution of resistance to ALS indicated a decreasing resistance with increased distance from an epicenter. After finer-scale analysis, less than 0.05% of the residual variation could be attributed to spatial autocorrelation. The spatial resistance pattern was not correlated with the dominant wind direction, while there was a correlation between the resistant phenotype and type of crop. This study underlines that NTSR mechanisms do not always confer broad resistance to different herbicide subclasses and site of action, hence the complex relationship to resistant phenotype. NTSR mechanisms, in particular detoxification, were present at different levels for the herbicides tested in the silky windgrass populations of this study. The factors contributing to the spatial distribution of resistance remain elusive.

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.

Dinitroanilines are microtubule inhibitors, targeting tubulin proteins in plants and protists. Dinitroaniline herbicides, such as trifluralin, pendimethalin and oryzalin, have been used as pre-emergence herbicides for weed control for decades. With widespread resistance to post-emergence herbicides in weeds, the use of pre-emergence herbicides such as dinitroanilines has increased, in part, due to relatively slow evolution of resistance in weeds to these herbicides. Target-site resistance (TSR) to dinitroaniline herbicides due to point mutations in α-tubulin genes has been confirmed in a few weedy plant species (e.g., Eleusine indica , Setaria viridis , and recently in Lolium rigidum ). Of particular interest is the resistance mutation Arg-243-Met identified from dinitroaniline-resistant L. rigidum that causes helical growth when plants are homozygous for the mutation. The recessive nature of the TSR, plus possible fitness cost for some resistance mutations, likely slows resistance evolution. Furthermore, non-target-site resistance (NTSR) to dinitroanilines has been rarely reported and only confirmed in Lolium rigidum due to enhanced herbicide metabolism (metabolic resistance). A cytochrome P450 gene (CYP81A10) has been recently identified in L. rigidum that confers resistance to trifluralin. Moreover, TSR and NTSR have been shown to co-exist in the same weedy species, population, and plant. The implication of knowledge and information on TSR and NTSR in management of dinitroaniline resistance is discussed.

Non-target site resistance (NTSR) to herbicides in black-grass ( Alopecurus myosuroides ) results in enhanced tolerance to multiple chemistries and is widespread in Northern Europe. To help define the underpinning mechanisms of resistance, global transcriptome and biochemical analysis have been used to phenotype three NTSR black-grass populations. These comprised NTSR1 black-grass from the classic Peldon field population, which shows broad-ranging resistance to post-emergence herbicides; NTSR2 derived from herbicide-sensitive (HS) plants repeatedly selected for tolerance to pendimethalin; and NTSR3 selected from HS plants for resistance to fenoxaprop- P -ethyl. NTSR in weeds is commonly associated with enhanced herbicide metabolism catalyzed by glutathione transferases (GSTs) and cytochromes P450 (CYPs). As such, the NTSR populations were assessed for their ability to detoxify chlorotoluron, which is detoxified by CYPs and fenoxaprop-P-ethyl, which is acted on by GSTs. As compared with HS plants, enhanced metabolism toward both herbicides was determined in the NTSR1 and NTSR2 populations. In contrast, the NTSR3 plants showed no increased detoxification capacity, demonstrating that resistance in this population was not due to enhanced metabolism. All resistant populations showed increased levels of Am GSTF1, a protein functionally linked to NTSR and enhanced herbicide metabolism. Enhanced Am GSTF1 was associated with increased levels of the associated transcripts in the NTSR1 and NTSR2 plants, but not in NTSR3, suggestive of both pre- and post-transcriptional regulation. The related HS, NTSR2, and NTSR3 plants were subject to global transcriptome sequencing and weighted gene co-expression network analysis to identify modules of genes with coupled regulatory functions. In the NTSR2 plants, modules linked to detoxification were identified, with many similarities to the transcriptome of NTSR1 black-grass. Critical detoxification genes included members of the CYP81A family and tau and phi class GSTs. The NTSR2 transcriptome also showed network similarities to other (a)biotic stresses of plants and multidrug resistance in humans. In contrast, completely different gene networks were activated in the NTSR3 plants, showing similarity to the responses to cold, osmotic shock and fungal infection determined in cereals. Our results demonstrate that NTSR in black-grass can arise from at least two distinct mechanisms, each involving complex changes in gene regulatory networks.