More Information on Herbicides, Herbicide Resistant Crops and DuPont Product Development

The five classes of ALS herbicides differ chemically, but all bind to the same target site on the ALS enzyme. The primary molecular basis of weeds resistant to ALS is reduction of target site sensitivity, although there are biotypes that are resistant through more rapid detoxification of the herbicide to inactive metabolites. Metabolic tolerance provided by detoxification generally results in lower levels of resistance than decreasing sensitivity to the herbicide through target site modifications.

To date, weed scientists have identified 92 weed species containing biotypes that are resistant to ALS herbicides (Heap, 2005). The large number of resistant biotypes is due, in part, to the relatively large number of amino acid substitutions that can change the ALS enzyme from a sensitive to a resistant form. Five different mutations sites have been identified in naturally occurring resistant weed populations (Bernasconi et al., 1995; Tranel and Wright, 2002). However, not all ALS resistant weeds are resistant to all classes of ALS herbicides (Tranel and Wright, 2002). ALSresistance generally falls into three categories:

1. broad resistance to sulfonylureas (SU), imidazolinones (IMI), triazolopyrimidines (TP), and pyrimidinylthiobenzoates (PTB);
2. resistance to IMI and PTB only; and
3. resistance to SU and TP only.  

Most ALS resistant weeds occur in small and localized areas only. Exceptions include ALS-resistant Kochia (Kochia scoparia) and Russian thistle (Salsola iberica), which are now present in over 60% of the wheat fields in northern United States (Heap and LeBaron, 2001), and ALS resistant water hemp in Illinois. As a consequence, few growers in these areas use ALS herbicides to control these weeds. However, they do apply ALS herbicides to control other weed species in their fields.