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Since their introduction in the mid-1920s, herbicides have become a fundamental tool for weed control in modern agricultural production systems. However, the continued use of herbicides with the same site of action has promoted the development and proliferation of resistant weeds in crop fields. In recent years, efforts to understand resistance mechanisms at the molecular level have become a key component in preventing the evolution of resistance. Both target-site resistance (TSR) and nontarget-site resistance (NTSR) mechanisms have been identified as the most common herbicide resistance mechanisms. TSR is usually characterized by mutations that affect the herbicide's target protein, limiting its access to the site of action. Most of these mutations occur either in or near the catalytic domain. Furthermore, increased copy numbers of the gene encoding the target protein and also involved in TSR resistance mechanisms. On the other hand, NTSR encompasses a broad range of resistance mechanisms, such as herbicide-enhanced metabolism, reduced uptake, and translocation. NTSR mechanisms typically involve multiple gene families, including, but not limited to, cytochrome P450, glutathione S-transferases, and others. Both TSR and NTSR mechanisms can coexist in the same plant, resulting in an evolutionary process that leads to the ineffectiveness of one or more herbicides with different modes of action.
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