Abstract

To gain some insight into the surprisingly frequent occurrence of multiple herbicide resistant wild oat in western Canada, the inheritance of multiple herbicide resistance was studied in two wild oat (Avena fatua L.) populations, UMWO12-01 and UMWO12-03, from Manitoba, Canada. Both populations are resistant to each of three distinct herbicides, imazametha benz-methyl, flamprop-methyl, and fenoxaprop-p-ethyl (hereafter referred to as imazamethabenz, flamprop, and fenoxaprop-P, respectively). Crosses were made between each resistant (R) population and a susceptible (S) wild oat population (UM5) (R/S crosses), and between the two resistant populations (R/R crosses). Subsets of parental, F2 plants, and F2-derived F3 (F2:3) families were treated separately with each of the three herbicides and classified as R or S for individual plants, and homozygous R, segregating, or homozygous S for F2:3 families. F2 plants and F2:3 families from R/S crosses segregated in 3R:1S and 1 homozygous R:2 segregating:1 homozygous S ratios, respectively. These ratios indicate that a single dominant or semi-dominant nuclear gene controls resistance to each of these herbicides in each population. F2 plants and F2:3 families from R/R crosses segregated for resistance/susceptibility when treated with either imazamethabenz or flamprop. Therefore, the genes for resistance to these two herbicides are different in each R population. Individual F2:3 family response demonstrated that the genes were not independent of each other, indicating possible linkage between the genes for resistance to each herbicide. Genetic linkage could explain how the wild oat populations developed multiple resistance in the absence of selection by two of the herbicides, imazamethabenz and flamprop. Key words: Wild oat, Avena fatua, herbicide resistance, genetics of resistance, multiple resistance

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