Weed resistance to herbicides states: Causes and possibilities of preventive resistance

Abstract

Resistance occurs as a result of heritable changes to biochemical processes that enable plant survival when treated with a herbicide. Resistance can result from changes to the herbicides target site such that binding of the herbicide is reduced, or over-expression of the target site may occur. Alternatively, there may be a reduction in the amount of herbicide that reaches the target enzyme through detoxication, sequestration, or reduced absorption of herbicide. Finally, the plant may survive through the ability to protect plant metabolism from toxic compounds produced as a consequence of herbicide action. Herbicide-resistant weeds were predicted shortly after the introduction of herbicides. During the 1970s, many, additional important weed species (e.g., Amaranthus spp., Chennpodium spp., Erigeron canadensis Kochia scoparia, Solanum nigrum, Panicum crus-galli, Senecio vulgaris, Poa annua) were reported to be resistant to triazine herbicides and several other herbicides. Over the last 10 years and now ALS-herbicide-resistant weeds account for the greatest number of resistant species and probably the largest area affected by resistance. In contrast to triazine resistance target-site-based resistance to the ALS-inhibiting herbicides can be conferred by a number of different point mutations. Differences occur in target-site cross-resistance among the different chemical classes of herbicides that inhibit ALS. The differences are related to particular amino acid substitutions that occur within the binding region. Indeed, six different substitutions of Ala, Arg, Glu, Leu, Ser, or Tri for Pro 173 have been observed in different weed populations.