Global warming will increase the incidence of metabolism-based reduced herbicide efficacy on weeds and, therefore, the risk for evolution of non-target site herbicide resistance. Climate changes affect food security both directly and indirectly. Weeds are the major biotic factor limiting crop production worldwide, and herbicides are the most cost-effective way for weed management. Processes associated with climatic changes, such as elevated temperatures, can strongly affect weed control efficiency. Responses of several grass weed populations to herbicides that inhibit acetyl-CoA carboxylase (ACCase) were examined under different temperature regimes. We characterized the mechanism of temperature-dependent sensitivity and the kinetics of pinoxaden detoxification. The products of pinoxaden detoxification were quantified. Decreased sensitivity to ACCase inhibitors was observed under elevated temperatures. Pre-treatment with the cytochrome-P450 inhibitor malathion supports a non-target site metabolism-based mechanism of herbicide resistance. The first 48 h after herbicide application were crucial for pinoxaden detoxification. The levels of the inactive glucose-conjugated pinoxaden product (M5) were found significantly higher under high- than low-temperature regime. Under high temperature, a rapid elevation in the level of the intermediate metabolite (M4) was found only in pinoxaden-resistant plants. Our results highlight the quantitative nature of non-target-site resistance. To the best of our knowledge, this is the first experimental evidence for temperature-dependent herbicide sensitivity based on metabolic detoxification. These findings suggest an increased risk for the evolution of herbicide-resistant weeds under predicted climatic conditions.
Pesticide efficacy is strongly associated with environmental conditions. Conditional resistance defined as a reduction in pesticide sensitivity under changed environmental conditions has been widely detected under climatic changes such as elevated temperatures and CO enrichment. Given the effects of environmental conditions on pesticide sensitivity, many of the putative resistance reports made by farmers may be due to pesticide application followed by non-optimal environmental conditions rather than the evolution of resistance. This type of conditional resistance may be the result of phenotypic plasticity or epigenetic changes in response to environmental changes. Elevated temperatures and CO enrichment can directly lead to reduced pesticide efficacy by altering pesticide metabolism and translocation, or indirectly increasing pesticide detoxification in host-plants thus reducing pesticide availability for the target pest. Stress-related signal transduction pathways, as well as physiological changes, can both be associated with accelerated pesticide detoxification under climatic changes. The possibility for parallel mechanisms controlling these responses in different pest species should be considered. It is proposed that the same mechanisms leading to non-target site resistance in pests may also play a role in conditional resistance, suggesting we can predict the pesticides to which pests are likely to be less responsive under changing climatic conditions. Using adjuvants to improve pesticide translocation or reduce pesticide metabolism, alongside with new technologies such as using nanoparticles may result in higher pesticide functionality under the projected climate change. Exploring the physiological, transcriptional and biochemical basis underlying conditional resistance is crucial in maintaining future pest management under changing environmental conditions. © 2018 Society of Chemical Industry.
Herbicides are the most commonly used means of controlling weeds. Recently, there has been growing concern over the potential impacts of global climate change, specifically, increasing temperatures and elevated carbon dioxide (CO2) concentrations, on the sensitivity of weeds to herbicides. Here, glyphosate response of both Conyza canadensis and Chenopodium album was evaluated under different environmental conditions. Reduced glyphosate sensitivity was observed in both species in response to increased temperature, elevated CO2 level, and the combination of both factors. Increased temperature had greater effect on plant survival than elevated CO2 level. In combination, high temperature and elevated CO2 level resulted in loss of apical dominance and rapid necrosis in glyphosate-treated plants. To investigate the mechanistic basis of reduced glyphosate sensitivity, translocation was examined using 14C-glyphosate. In plants that were subjected to high temperatures and elevated CO2 level, glyphosate was more rapidly translocated out of the treated leaf to shoot meristems and roots than in plants grown under control conditions. These results suggest that altered glyphosate translocation and tissue-specific sequestration may be the basis of reduced plant sensitivity. Therefore, overreliance on glyphosate for weed control under changing climatic conditions may result in more weed control failures.
Distribution of Conyza species is well correlated with human interference. Multiple herbicide resistance is caused by the attempt to overcome resistance to one mode of action by overuse of another. Conyza canadensis (CC) and Conyza bonariensis (CB) are troublesome weeds around the world. Extensive use of herbicides has led to the evolution of numerous Conyza spp. herbicide-resistant populations. Seeds of 91 CC and CB populations were collected across Israel. They were mostly found (86 %) in roadsides and urban habitats, two disturbed habitats that had been dramatically impacted by human activities, thus we classify these species as anthropogenic. Although pyrithiobac-sodium was only used in cotton fields, 90 % of Conyza spp. populations were identified as pyrithiobac-sodium resistant, suggesting possible natural resistance to pyrithiobac-sodium. CC21 and CC17 C. canadensis populations were highly resistant to all tested ALS inhibitors due to a substitution in the ALS gene from Trp574 to Leu. They were also atrazine resistant due to a substitution in the psbA gene from Ser264 to Gly. The high level of imazapyr and pyrithiobac-sodium resistance observed in the CC10 population was due to an Ala205 to Val substitution. However, high resistance to sulfometuron methyl and pyrithiobac-sodium in population CC6 was due to a point mutation at Pro197 to Ser. All resistant plants of CC21 population showed both psbA (Ser264 to Gly) and ALS (Trp574 to Leu) substitutions, leading us to the conclusion that the attempt to overcome resistance to one mode of action by overuse of another will most likely lead to multiple herbicide resistance. Furthermore, we concluded that only individuals that carry both mutations could survive the shift between the two modes of action and overcome the fitness cost associated with the PSII resistance.
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