Weed Resistance to Herbicides

Abstract

Unfortunately, herbicide resistance developed shortly after the introduction of the herbicides 2,4-D in 1957. According the herbicide resistance mechanisms, all processes can be grouped as follows: target-site resistance, non-target-site resistance, cross-resistance and multiple-resistance. Target-site resistance is generally due to a single or several mutations in the gene encoding the herbicide-target enzyme, which, in turn, decreases the affinity for herbicide binding to that enzyme. Non-target-site resistance is caused by mechanisms that reduce the amount of herbicidal active compound before it can attack the plant through the reduced absorption or altered translocation, increased herbicide sequestration or enhanced herbicide metabolism. Cross-resistance means that a single-resistance mechanism causes resistance to several herbicides with some mode of action. Multiple-resistance is a situation where two or more resistance mechanisms are present within the same plant, often due to sequential selection by herbicides with different modes of action. Currently, herbicide resistance has been reported in 478 weed biotypes (252 weed species) in 67 countries. Many of those biotypes are resistant to acetolactate synthase (ALS) inhibitors, PS II inhibitors, ACC-ase inhibitors and EPSPS inhibitors. Strategy for herbicide-resistance weed management must involve all the available preventive, cultural, mechanical and chemical measures for effective, safe and cost-effective weed control.

Origanum vulgare essential oils inhibit glutamate and aspartate metabolism altering the photorespiratory pathway in Arabidopsis thaliana seedlings

“…Furthermore, both the sesquiterpene trans-caryophyllene and the monoterpene citral alter the plant water status inhibiting the germination and growth of several weeds (Araniti et al 2017b;Graña et al 2016), whereas the monoterpene 1,8-cineole strongly inhibits all the mitosis phases and the respiration of isolated organelles (Romagni et al 2000). The high variety of combinations of different terpenoids, with diverse biological activity, in EOs composition, could be really interesting to develop new multi-targeted bio-herbicides as it allows: 1) the synergistic interaction among their components, increasing the biological activity (Araniti et al 2013a;Andrés et al, 2017); 2) the trigger of phytotoxic activity of compounds present at non-phytotoxic concentration and/or sometimes in traces (Araniti et al 2013a); 3) the overcome of resistance phenomenon to the synthetic herbicides (Vrbničanin et al 2017). As reported by Holt et al (1993), the classes of herbicides against which resistance is largely increasing tend to have single target sites under the control of single or very few genes.…”

Journal of Plant Protection Research

“…In addition, Baucom (2019) reported that natural selection processes where genetic mutations occur naturally in plants due to continuous use of similar herbicides will stimulate weed resistance. Weeds that survive will persistantly reproduce, whereas weeds that are susceptible to herbicides will die in the presence of herbicides (Vrbničanin et al 2017). In general, based on the dry weight of weeds, weeds that are exposed to herbicides have a lower average of weed growth reduction than weeds that are not exposed to herbicides.…”

Efficacy of Reduced Rates of Soil-Applied Dimethenamid-P and Pendimethalin Mixture Followed by Postemergence Herbicides in Maize

“…A single herbicide does not usually control all weeds species; therefore, combination of herbicides or sequential treatments are required. Properly selected herbicides, especially those containing substances with different sites of action, allow effective control over a wide range of weed species, and it is an element of strategy for herbicide-resistance weed management [36]. The mixtures of herbicides at reduced rates can be an effective strategy to manage the problem of resistance development in weeds but only when they are really as effective as herbicides applied at label rates.…”