Resistance to aryloxyphenoxypropionate and cyclohexanedione herbicides was identified in four wild oat populations from western Canada. Populations UM1, UM2, and UM3 originated from northwestern Manitoba and UM33 from south-central Saskatchewan. Field histories indicated that these populations were exposed to repeated applications of diclofop-methyl and sethoxydim over the previous 10 yr. The populations differed in their levels and patterns of cross-resistance to these and five other acetyl-CoA carboxylase inhibitors (ACCase inhibitors). UM1, UM2, and UM3 were resistant to diclofop-methyl, fenoxaprop-p-ethyl, and sethoxydim. In contrast, UM33 was resistant to the aryloxyphenoxy propionate herbicides but not to sethoxydim. The dose of sethoxydim required to reduce growth of UM1 by 50% was 150 times greater than for a susceptible population (UM5) or UM33 based on shoot dry matter reductions 21 d after treatment. This population differed from UM2 and UM3 that had R/S ratios of less than 10. In the field UM1 also exhibited a very high level of resistance to sethoxydim. In contrast to susceptible plants that were killed at the recommended dosage, shoot dry matter of resistant plants treated at eight times the recommended dosage was reduced by only 27%. In growth chamber experiments none of the four populations was cross-resistant to herbicides from five different chemical families.

A seed bioassay was developed and tested for the rapid identification of aryloxyphenoxypropionate (APP) and cyclohexanedione (CHD) resistance in wild oat. Two susceptible (S) genotypes, UM5 and Dumont, were treated with fenoxaprop-P and sethoxydim over a range of dosages on filter paper and agar. The former is a wild oat line and the latter a tame oat cultivar. Within 5 d, shoot and root development of both genotypes were completely inhibited by 10 μM fenoxaprop-P and 5 μM sethoxydim. These dosages were then tested to determine if they were suitable for distinguishing between resistant (R) and susceptible (S) plants. Agar medium was preferred over filter paper because of the ease of preparation and maintenance. Four known R wild oat populations were included in the tests. Those with high levels of resistance produced significantly longer coleoptiles and roots than S genotypes, but those with moderate or low levels of resistance could not be separated statistically from S biotypes based on quantitative measurements. However, after exposing the germinating, treated seeds to light for 24 to 48 h, all the R populations produced green coleoptiles and initiated a first leaf, unlike the S genotypes which did not turn green or produce any new growth. This procedure proved useful in discriminating between R and S genotypes and in ranking populations in terms of relative levels of resistance.

Resistance to fenoxaprop-P and other aryloxyphenoxypropionate and cyclohexanedione herbicides in the wild oat population, UM1, is controlled by a single, partially dominant, nuclear gene. In arriving at this conclusion, parents, F1hybrids, and F2plants derived from reciprocal crosses between UM1 and a susceptible wild oat line, UM5, were treated with fenoxaprop-P over a wide range of dosages. Based on these experiments, a dosage of 400 g ai ha−1fenoxaprop-P was selected to discriminate between three response types. At this dosage, susceptible plants were killed and resistant plants were unaffected, whereas plants characterized as intermediate in response were injured but recovered. Treated F2plants segregated in a 1:2:1 (R, I, S) ratio, indicative of single nuclear gene inheritance. This was confirmed by selfing F2plants and screening several F3families. Families derived from intermediate F2plants segregated for the three characteristic response types, whereas those derived from resistant F2plants were uniformly resistant. Chisquare analysis indicated the F2segregation ratios fit those expected for a single partially dominant nuclear gene system. In addition, F2populations from both crosses were screened with a mixture of fenoxaprop-Pand sethoxydim. The dosages of both herbicides (150 g ai ha−1fenoxaprop-P and 100 g ha−1sethoxydim) were sufficient to control only susceptible plants. Treated F2populations segregated in a 3:1 (R:S) pattern, thereby confirming that resistance to the two chemically unrelated herbicides results from the same gene alteration.

Two separate field experiments were conducted to quantify the degree of plant-to-plant outcrossing and pollen-mediated gene flow (PMGF) in wild oat. The purpose of the study was to determine the extent to which pollen movement could contribute to the spread of herbicide resistance in this species. In both experiments, an acetyl-CoA carboxylase inhibitor–resistant (R) wild oat genotype (UM1) was used as the pollen donor and a susceptible (S) genotype (UM5) was used as the pollen receptor. Hybrid progeny resulting from a cross between UM1 and UM5 were identified using the herbicide resistance trait as a marker. In the plant-to-plant outcrossing experiment, single UM5 plants were closely surrounded by 20 homozygous R UM1 plants in hills. By screening seed from the S parent for resistance, outcrossing was determined to range from 0 to 12.3%, with a mean of 5.2% over 10 hills. In the PMGF experiment, single homozygous R UM1 plants were surrounded by UM5 plants arranged in a hexagonal pattern at low and high densities (total of 19 and 37 wild oat plants m−2), growing within spring wheat and flax crops. In the wheat crop, mean wild oat outcrossing was 0.08 and 0.05% at low and high densities, respectively. In the less competitive flax, corresponding outcrossing values were 0.07 and 0.16% at low and high densities, respectively. Distance from the pollen source was a significant factor only for the high-density planting arrangement in flax. Up to 77 R hybrid seeds were recovered from 6 m2 in the PMGF experiment, indicating that PMGF contributes to the evolution of resistance in wild oat populations. However, the contribution of pollen movement to resistance evolution and the spread of resistance in wild oat populations would be relatively small when compared with R seed production and dispersal from a resistant plant. EDITOR'S NOTE: This manuscript was reviewed by six colleagues whose recommendations varied widely. Lack of repetition was a major concern. The authors address the problem in the last paragraph of the results section. Factors favoring publication included the worldwide importance of wild oats, the minimal data on gene flow in the species, and the fact that the results are consistent with those of other studies cited in this manuscript. The points raised by reviewers who did not favor publication, especially the role of the environment in pollen production and viability, are acknowledged. R. L. Zimdahl, Editor

Extensive use of the preemergence herbicide triallate over the last three decades has selected for resistant (R) Avena fatua L. populations in several areas of the United States and Canada. R plants are also cross-resistant to the unrelated pyrazolium herbicide difenzoquat. We made reciprocal crosses between inbred R and susceptible (S) lines to determine the genetic basis of triallate resistance. Seeds from parental lines and F(2) populations were treated with soil applications of 0.275, 0.55, or 1.1 kg/ha triallate in the greenhouse and plant heights recorded after 37 days. Surviving F(2) plants were selfed and the resulting F(3) families were screened with 1.1 kg/ha triallate. In the F(2) populations, assortment of S and R phenotypes fit a 15:1 segregation ratio, suggesting that resistance was controlled by the two independently segregating recessive genes TRR1 and TRR2. None of the 912 F(3) progeny from 51 R F(2) individuals was susceptible to triallate treatment, further supporting a two-gene mode of inheritance. There was a possible maternal effect on susceptibility at the highest triallate rate tested.