Cross resistance of herbicide resistant weeds to ALS-inhibitors

We discussed management strategies to reduce selection pressure for ALS-resistance in ICM newsletter IC-466(26). Annual rotation of different herbicide classes was suggested. However, the effectiveness of rotating ALS-inhibitors is questionable because three distinct classes of chemistry inhibit the ALS enzyme (Table 1, opposite page).

Altering the active site on the ALS enzyme that prevents binding of the herbicide causes ALS resistance. Differences in molecular structure cause some ALS inhibitors to bind at slightly different locations on the enzyme than do others. Several modifications of the ALS enzyme that provide resistance to ALS inhibiting herbicides have been identified. A specific alteration of the ALS enzyme may affect herbicide binding sites differently and provide resistance to certain herbicides (Figure 1, opposite page).

A weed is cross resistant if it resists several herbicides. Cross resistance to ALS inhibitors is complicated by multiple binding sites and multiple enzyme modifications. The degree of cross resistance has varied widely among different ALS resistant weeds. For example, some biotypes of Scepter-resistant cocklebur, which were identified in the Mississippi Delta and Missouri, are also resistant to Classic and Broadstrike. Other Scepter resistant biotypes remain susceptible to these herbicides.

If a weed biotype is cross resistant to several ALS inhibitors, rotating these products will not delay the onset of resistance. Since it is not possible to predict the occurrence of cross resistance in weed populations, we suggest that you not rotate different ALS inhibitors as a resistance management strategy.

Updated 02/24/1994 - 1:00pm