Through the repeated use of herbicides with similar modes of action, i.e., on the same site, selection for increased resistance within existing weed populations has been imposed. The result is the development of species or biotypes that can no longer be controlled with some selective herbicides. There has been a dramatic increase in the incidence of herbicide resistance. There are over 100 weed species where herbicide resistant biotypes have been reported. Triazine resistance is the most prevalent.
Pigweed
One of the best examples of a weed that has readily developed resistance to herbicides such as the triazines is the pigweeds. In 1979, triazine-resistant pigweed was found along railroad right-of-ways from Nebraska to Washington. Another example is kochia and by 1981, commercial applicators and growers were reporting field infestations of kochia that were no longer effectively controlled by normal use rates of atrazine.
No-till or reduced tillage systems rely heavily on atrazine for chemical weed control. Many of the fields where triazine resistant kochia was found, were located along a road, railroad right-of-way or industrial site that had used a soil sterilant for many years.
Recently, an increasing number of weed species have developed resistance to herbicides other than the triazines. In 1987, weed species in seven locations in Idaho, North Dakota, Kansas, and Colorado were found to be resistant to a sulfonylurea herbicide. Weeds showing resistance were prickly lettuce and kochia. By the end of 1989, resistance to the sulfonylurea herbicides had been documented at 111 locations, 89 of which were agricultural sites, spread over 10 U.S. states and two Canadian provinces. Like triazine-resistance biotypes, the resistant biotypes usually show varying degrees of cross resistance to other chemical in the same herbicide family. The recent discovery of multiple resistance to several different classes of herbicides has also become a major concern.
The sulfonylurea and imidazolinone herbicides have the same mode of action. They both inhibit the action of the acetolactase synthase (ALS) enzyme. This enzyme is needed for the production of essential amino acids required for cell development in plants. Many herbicides introduced since the 1990s belong to one of these two herbicide classes. The potential to develop weed resistance to these herbicides is high where an ALS-inhibiting herbicide is marketed in more than one crop in a two to three year crop rotation, e.g. corn-soybean rotations. The release of crops resistant to ALS-inhibiting herbicides, e.g. corn varieties, increases the likelihood of continuous use of herbicides with the same mode of action.
Resistance has not appeared to the phenoxy herbicides (In actuality, they are plant growth regulators.) despite monoculture with continuous use of 2,4-D for more than 30 years. This rapidly degraded herbicide has a much lower effective kill (the ability to control a weed and prevent seed production over the growing season) than the triazines. The phenoxy herbicides also have a completely different and complex, probably multi-site, mechanism of action. 2,4-D is a synthetic analog of a naturally-occurring plant hormone, IAA, an auxin. It acts as herbicide by giving a plant too much hormonal activity in the wrong places, causing the plant to mis-shape and be unable to compete for nutrients.
If a herbicide-resistant weed population is identified and confirmed, it is important to determine the extent of its distribution within the immediate area. It may be possible to contain a small infestation of the species to one farm or one field. Quarantine methods are recommended in such cases whenever feasible. Other control measures include substituting herbicides in an existing cropping system, altering tillage operations, the use of herbicides applied at different times during the cropping season, and crop rotations.
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