ABSTRACT
In the 25 years since the discovery of the simazine-resistant S. vulgaris, there have been numerous reports of weed biotypes exhibiting resistance to Photosystem (PS) II inhibiting herbicides. Herbicide resistance in weeds can be due to a number of mechanisms: modified target site, enhanced detoxification, reduced absorption/translocation, sequestration or compartmentation, and repair of the toxic effects of herbicides. Preliminary indications are that this type of resistance is not associated with reduced ecological fitness. Alternatively, resistance to PS II inhibitors could be conferred by the introduction of nuclear genes encoding herbicide detoxifying enzymes. During the 1980s, resistance to PS II inhibiting herbicides due to enhanced metabolism appeared in weeds. The approximately 200-ha farm on which the triazine-resistant A. theophrasti was found is now heavily infested with this weed and other herbicide classes are used to control it. The nature of the problem has been best characterized for the resistant A. myosuroides biotypes found in England.
