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

ALS-inhibiting herbicides were discovered in 1975 (Stetter, 1994; Shaner and O’Connor, 2000; Tan et al., 2005). They inhibit a plant enzyme called acetolactate synthase (ALS) that is required for the production of essential branched-chain amino acids such as valine, leucine, and isoleucine. This biochemical pathway is not present in humans and animals (Saari and Mauvais, 1996). There are five different chemical classes of ALS herbicides (sulfonylureas (SU), imidazolinones (IMI), triazolopyrimidines (TP), pyrimidinylthiobenzoates (PTB), and sulfonylamino-carbonyl-triazolinones (SCT).

ALS herbicides control a wide spectrum of grass and broadleaf weeds at very low application rates. In addition, they generally have very low mammalian toxicity and possess a favorable environmental profile. Today, about 56 different ALS herbicide active ingredients are marketed with registrations in all major crops. Significant changes in herbicide potency, crop selectivity, and weed control can be made with small chemical alterations within the ALS herbicide class.

Soon after the commercialization of the first ALS herbicides, tissue culture was used to successfully select highly tolerant tobacco lines (Chaleff and Ray, 1984). The development of ALS-resistant corn began in 1982 with tissue culture selection of corn callus after exposure to the imidazoline herbicide, imazaquin. This process resulted in several imidazolinone-tolerant cell lines. Two of those lines, XA17 and XI12, were regenerated into mature corn plants and the imidazoline tolerance trait was introduced into commercial corn varieties through breeding.

In both XA17 and XI12, resistance is due to a change in single amino acids that alters the ability of the herbicide to bind to its target site, the ALS enzyme. Other independently discovered imidazoline-resistance traits obtained through corn tissue culture selection are also single nucleotide changes, leading to an amino acid substitution. Typically, they only provide increased tolerance to a single class of ALS- inhibiting herbicides, the imidazolines.

Also in 1980s, breeders introduced genetic variation into soybean seeds and subsequently screened for those that emerged into sulfonylurea resistant plants. One plant showed significant increase in SU resistance, as a result of a single amino acid mutation in the ALS enzyme (Sebastian et al., 1989). The progeny of this plant was utilized in breeding programs to incorporate the trait into a wide range of agronomically useful soybean varieties, which became commercially available in 1993 as STS® soybeans (Sulfonylurea tolerant soybeans).

Shortly thereafter, a further improved source of ALS resistance was discovered in corn and soybeans, a double mutant ALS allele that encodes for a highly resistant form of the ALS enzyme (HRA; highly resistant allele) (Lee et al., 1988; Mazur and Falco, 1989; Bedbrook et al., 1995). The HRA trait is dominant and is expressed throughout the plant, so ALS herbicides do not harm plant roots or shoots.

The two mutations in the double mutant are also amino acid substitutions, but the locations of the substitutions vary slightly depending on the plant source. The two mutations provide different types of resistance to ALS herbicides (Tranel and Wright, 2002), with one giving broad-spectrum resistance to ALS herbicides, while the other one confers resistance to sulfonylureas and triazolopyrimidines. Both mutations together, as present in the double mutant, provide resistance to all five classes of ALS herbicides. When HRA is adequately expressed in plants, high rates of ALS herbicides can be applied without crop injury.

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