Glufosinate-resistant Lolium perenne L. spp. multiflorum biotypes from Oregon exhibited resistance levels up to 2.8-fold the field rate. One resistant biotype (MG) had an amino acid substitution in the glutamine synthetase 2 (GS2), whereas the other (OR) exhibited the wild-type genotype. We hypothesized that the amino acid substitution in GS2 is involved in the resistance mechanism in MG, and that non-target site resistance mechanisms are present in OR. OR metabolized glufosinate faster than the other two biotypes, with >75% of the herbicide metabolized, compared to 50% in MG and the susceptible biotype. A mutation in the GS2 co-segregating with resistance in MG did not reduce the enzyme activity, results further supported by our enzyme homology models. This research supports the conclusion that a metabolism mechanism of glufosinate resistance is present in OR, and that glufosinate resistance in MG is not due to an altered target-site.
TheLoliumgenus encompasses many species that colonize a variety of disturbed and non-disturbed environments.Lolium perenneL. spp.perenne,L.perenneL. spp.multiflorum, andL.rigidumare of particular interest to weed scientists because of their ability to thrive in agricultural and non-agricultural areas. Herbicides are the main tool to control these weeds; however,Loliumspp. populations have evolved multiple- and cross-resistance to at least 14 herbicide mechanisms of action in more than 21 countries, with reports of multiple herbicide resistance to at least seven mechanisms of action in a single population. In this review, we summarize what is currently known about non-target-site resistance inLoliumspp. to acetyl CoA carboxylase, acetohydroxyacid synthase, microtubule assembly, photosystem II, 5-enolpyruvylshikimate-3-phosphate synthase, glutamine synthetase, very-long chain fatty acids, and photosystem I inhibitors. We suggest research topics that need to be addressed, as well as strategies to further our knowledge and uncover the mechanisms of non-target-site resistance inLoliumspp.
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.
Lolium perenne L. spp. multiflorum (Lam.) Husnot (LOLMU) is a winter annual weed, common to row crops, orchards and roadsides. Glyphosate-resistant populations of LOLMU are widespread in California. In many situations, growers have switched to paraquat or other postemergence herbicides to manage glyphosate-resistant LOLMU populations. Recently, poor control of LOLMU with paraquat was reported in a prune orchard in California where paraquat has been used several times. We hypothesize that the low efficacy observed is due to the selection of a paraquat-resistant biotype of LOLMU. Greenhouse dose-response experiments conducted with a susceptible (S) and the putative paraquat-resistant biotype (PRHC) confirmed paraquat resistance in PRHC. Herbicide absorption studies indicated that paraquat is absorbed faster in S than PRHC, although the maximum absorption estimates were similar for the two biotypes, indicating that differential foliar absorption of paraquat is not the cause of the resistance. Conversely, translocation of 14C-paraquat under light-manipulated conditions was restricted to the treated leaf of PRHC, whereas herbicide translocation out of the treated leaf was nearly 20 times greater in S. These results suggest that paraquat was either restricted to the apoplast or was compartmentalized within the plant cell but away from the chloroplast in PRHC. To determine whether paraquat was active within the plant cells, the photosynthetic performance was assessed after paraquat application using the parameter maximum quantum yield of photosystem II (Fv/Fm). Results indicated that paraquat reaches the chloroplasts of PRHC, since there was a transitory inhibition of photosynthetic activity in PRHC leaves. However, PRHC Fv/Fm recovered to initial levels by 48 hours after paraquat treatment. No paraquat metabolites were found, indicating that paraquat is stable in LOLMU plant cells and resistance is not likely due to paraquat degradation. LOLMU leaf segments were exposed to paraquat following pretreatments with inhibitors of plasma membrane- and tonoplast-localized transporter systems to selectively block paraquat intracellular movement. Subsequent evaluation of membrane integrity indicated that pre-exposure to putrescine resulted in the resistant biotype responding to paraquat similarly to S. These results strongly indicate that vacuolar sequestration is involved in the resistance to paraquat in this population of LOLMU.