SummaryThe feasibility of achieving selective wild oat (Avena fatuaL.) control in a stand of the Australian oat (Avena sativaL.) cv. Savena I was examined. Diclofop‐methyl was applied at rates of 0·4–0·7 kg a.i. ha−1at the three‐ and five‐leaf stages ofA. fatua(84–132 culms m2). Although all rates of diclofop‐methyl caused initial chlorosis and necrosis to the crop, the subsequent control ofA. fatuapermitted increased crop tillering.Avena fatuacontrol and crop yield response were maximized when diclofop‐methyl was applied at the three‐leaf stage. Crop grain yield was increased by as much as 32% and 22% during 1984 and 1985, respectively. In the absence ofA. fatuacompetition, crop shoot dry weight at ear emergence was reduced only where diclofop‐methyl was applied at 0·6 or 0·7 kg ha−1. However, final grain yield was not reduced by any treatment. Only 11 of 240 cultivars or lines tolerated diclofop‐methyl, and none reached the level attained by Savena I and a closely related Australian line [(Irwin × (West × New Zealand Cape/42)) × West]/24. The nature of the inheritance of diclofop‐methyl tolerance was examined (1983–1985) by crossing and backcrossing (BC) Savena I with four diclofop‐methyl susceptible, but agronomically superior, lines. Inheritance of diclofop‐methyl tolerance appeared to be controlled by two genes, with susceptibility being dominant t