The importance of various factors influencing the evolution of herbicide resistance in weeds is critically examined using population genetic models. The factors include gene mutation, initial frequency of resistance alleles, inheritance, weed fitness in the presence and absence of herbicide, mating system, and gene flow. Where weed infestations are heavy, the probability of selecting for resistance can be high even when the rate of mutation is low. Subsequent to the occurrence of a resistant mutant, repeated treatments with herbicides having the same mode of action can lead to the rapid evolution of a predominantly resistant population. At a given herbicide selection intensity, the initial frequency of resistance alleles determines the number of generations required to reach a specific frequency of resistant plants. The initial frequency of resistance alleles has a greater influence on the evolutionary process when herbicides impose weak selection, as opposed to very strong selection. Under selection, dominant resistance alleles increase in frequency more rapidly than recessive alleles in random mating or highly outcrossing weed populations. In highly self-fertilizing species, dominant and recessive resistance alleles increase in frequency at approximately the same rate. Gene flow through pollen or seed movement from resistant weed populations can provide a source of resistance alleles in previously susceptible populations. Because rates of gene flow are generally higher than rates of mutation, the time required to reach a high level of resistance in such situations is greatly reduced. Contrary to common misconception, gene flow from a susceptible population to a population undergoing resistance evolution is unlikely to slow the evolutionary process significantly. Accurate measurements of many factors that influence resistance evolution are difficult, if not impossible, to obtain experimentally. Thus, the use of models to predict times to resistance in specific situations is markedly limited. However, with appropriate assumptions, they can be invaluable in assessing the relative effectiveness of various management practices to avoid, or delay, the occurrence of herbicide resistance in weed populations.

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.

The inheritance of resistance to dicamba in wild mustard was determined by making reciprocal crosses between a resistant (R) population derived from a field treated repeatedly with auxin-type herbicides, and a known susceptible (S) population. The resulting F1 hybrids were selfed to produce F2 populations and backcrossed to the S parent. At the three- to four-leaf stage, parental, F1, F2, and backcross populations were screened for resistance to dicamba at three dosages (50, 200, and 400 g ai ha−1). F1 progeny survived all dosages and exhibited levels of injury similar to the R parental population. F2 populations segregated in a 3:1 ratio of R to S phenotypes. Progeny of backcrosses segregated in a 1:1 (R:S) ratio. Responses of the F1, F2, and backcross populations to treatment with dicamba indicate that resistance is determined by a single, completely dominant nuclear allele.

R3T2N2; and 2Research Station, Agriculture Canada, Regina, Saskatchewan S4P 3A2. Contibutionno.654', received I3 Sept. 1984, accepted22 Feb. 1985 Douclns, BnreN J., Tuorvres, A. GonooN, MonnrsoN, IaN N. eNo For personal use only.

Developing aleurone cells can first be distinguished 10 days after anthesis beneath the degenerating nucellus as somewhat cuboidal cells with extremely thin walls and large nuclei. Ribosomes are very abundant but little endoplasmic reticulum (ER) is apparent. By 14 days the cell walls are intensely autofluorescent, possibly due to the presence of a ferulic acid-carbohydrate complex. At this stage the cytoplasm is characterized by the presence of large vacuoles, many of which contain small, electron-dense inclusions, presumably the beginnings of the phytin globoids (Type I inclusions) of mature aleurone grains. The paired appearance of many of the cells suggests that they are dividing periclinally, the innermost cells destined to become part of the starchy endosperm. By 4 weeks the cell walls have greatly thickened, ER and mitochondria have proliferated, and the vacuoles, which subsequently give rise to mature aleurone grains, contain a second type of inclusion (Type II inclusion) embedded in a protein matrix. Although the walls remain uniformly autofluorescent, an intensely stained inner wall can be distinguished readily from the outer wall. By 5 weeks the aleurone grains are almost completely surrounded by lipid droplets and contain numerous Type I inclusions. The cells change little in appearance from 6 weeks to maturity. At the latter stage the inner and outer walls are quite distinct and the cytoplasm is densely packed with aleurone grains which are completely surrounded by lipid droplets and interspersed with occasional plastids and numerous mitochondria with rather indistinct cristae.