Many herbicide-resistant weed species are polyploids, but far too little about the evolution of resistance mutations in polyploids is understood. Hexaploid wild oat (Avena fatua) is a global crop weed and many populations have evolved herbicide resistance. We studied plastidic acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicide resistance in hexaploid wild oat and revealed that resistant individuals can express one, two or three different plastidic ACCase gene resistance mutations (Ile-1781-Leu, Asp-2078-Gly and Cys-2088-Arg). Using ACCase resistance mutations as molecular markers, combined with genetic, molecular and biochemical approaches, we found in individual resistant wild-oat plants that (1) up to three unlinked ACCase gene loci assort independently following Mendelian laws for disomic inheritance, (2) all three of these homoeologous ACCase genes were transcribed, with each able to carry its own mutation and (3) in a hexaploid background, each individual ACCase resistance mutation confers relatively low-level herbicide resistance, in contrast to high-level resistance conferred by the same mutations in unrelated diploid weed species of the Poaceae (grass) family. Low resistance conferred by individual ACCase resistance mutations is likely due to a dilution effect by susceptible ACCase expressed by homoeologs in hexaploid wild oat and/or differential expression of homoeologous ACCase gene copies. Thus, polyploidy in hexaploid wild oat may slow resistance evolution. Evidence of coexisting non-target-site resistance mechanisms among wild-oat populations was also revealed. In all, these results demonstrate that herbicide resistance and its evolution can be more complex in hexaploid wild oat than in unrelated diploid grass weeds. Our data provide a starting point for the daunting task of understanding resistance evolution in polyploids.

Weed management is an arduous undertaking in crop production. Integrated weed management, inclusive of the application of bioherbicides, is an emerging weed control strategy toward sustainable agriculture. In general, bioherbicides are derived either from plants containing phytotoxic allelochemicals or certain disease-carrying microbes that can suppress weed populations. While bioherbicides have exhibited great promise in deterring weed seed germination and growth, only a few in vitro studies have been conducted on the physiological responses they evoke in weeds. This review discusses bioherbicide products that are currently available on the market, bioherbicide impact on weed physiology, and potential factors influencing bioherbicide efficacy. A new promising bioherbicide product is introduced at the end of this paper. When absorbed, phytotoxic plant extracts or metabolites disrupt cell membrane integrity and important biochemical processes in weeds. The phytotoxic impact on weed growth is reflected in low levels of root cell division, nutrient absorption, and growth hormone and pigment synthesis, as well as in the development of reactive oxygen species (ROS), stress-related hormones, and abnormal antioxidant activity. The inconsistency of bioherbicide efficacy is a primary factor restricting their widespread use, which is influenced by factors such as bioactive compound content, weed control spectrum, formulation, and application method.

The biochemical basis of resistance to the acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicide diclofop-methyl was investigated in a resistant wild oat population (R1), which does not exhibit a resistant ACCase. Rates of foliar uptake and translocation of [14C]-diclofop were the same in the R1 vs. susceptible (S) populations. However, the level of phytotoxic diclofop acid was always found to be lower in the R1 vs. S plants, with a concomitant higher level (up to 1.7-fold) of nontoxic polar diclofop metabolites in R1 relative to the S plants. These results indicate that a non–target-site-based mechanism of enhanced rate of diclofop acid metabolism confers resistance in population R1. Moreover, the high-performance liquid chromotography elution profile of the major diclofop metabolites in R1 is similar to that of wheat, suggesting resistance in individuals of population R1 involves a wheat-like detoxification system mediated by cytochrome P450 monooxygenases. In addition, lower level of tissue diclofop acid was also observed using nonradioactive ultra-performance liquid chromatography–mass spectrometry analysis in resistant individuals of three other resistant wild oat populations (R2, R3, and R4) known to posses ACCase gene resistance mutations. These results establish that either one or at least two independent resistance mechanisms (target-site ACCase resistance mutations and non–target-site enhanced rates of herbicide metabolism) can be present in individual wild oat plants.

Avenaspp. are world weeds with many cases of evolved herbicide resistance. In Australia,Avenaspp. (wild oat and sterile oat) are a major problem, especially in grain crops. Acetyl-CoA carboxylase (ACCase)–inhibiting herbicides have been used extensively since the late 1970s forAvenaspp. control. However, continued reliance on these herbicides has resulted in the evolution of resistantAvenaspp. populations. Resistance across many ACCase-inhibiting herbicides was characterized in fourAvenaspp. populations from the Western Australian grain belt. Dose–response experiments were conducted to determine the level of resistance to the aryloxyphenoxypropionates and cyclohexanediones and to the phenylpyrazoline herbicide pinoxaden. On the basis of resistance index values, all four resistant populations exhibited high-level diclofop resistance but varied in the level of resistance to other ACCase-inhibiting herbicides tested. It is evident thatAvenaspp. populations from the Western Australian grain belt have evolved resistance to a number of ACCase-inhibiting herbicides.