A single dominant mutation conferring resistance to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides was incorporated into a quantitative model for the population development of wild oat. The model was used to predict the times required to develop field resistance in a number of different scenarios. Field resistance was defined as a threshold of four plants m−2 surviving herbicide treatment, and in most scenarios, a very large proportion of these plants were resistant. The model predicts that plow cultivation could delay the development of resistance relative to tine cultivation. With an initial seed bank of 100 seeds m−2 and annual use of AOPP/CHD herbicides, which kill 90% of susceptible but no resistant plants, field resistance develops in 15 yr with annual tine cultivation 10 cm deep but only after 23 yr with annual plowing 20 cm deep. The model predicts that herbicide rotation can dramatically increase the times required for field resistance to develop in a tine cultivation system. With annual use of AOPP/CHD herbicides, field resistance develops in 15 yr, whereas using alternative modes of action 1 in 2 yr delays field resistance to 28 yr. The model predicts that resistance can be delayed for at least 66 yr if three herbicides, each with a different mode of action, are rotated and each herbicide causes 90% mortality. The model predictions on the number of years required for field resistance to develop are not highly sensitive to the initial density of the seed bank (range modeled = 102 to 104), the mutation rate for resistance (10−4 to 10−7 per generation), the rate of outcrossing (0.1 to 100%) or the herbicide kill rate (80 to 95%).
Nomenclature: Wild oat, Avena fatua L. AVEFA; aryloxyphenoxypropionate herbicide; cyclohexanedione herbicide.
