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BACKGROUND: Some herbicides are commercially formulated with safeners to increase crop selectivity. Fenoxaprop-p-ethyl is formulated with the safener isoxadifen-ethyl for Echinochloa crus-galli control in rice. Safeners act on crops by increasing herbicide metabolism, but this effect may also occur in weeds. The objective of this study was to investigate the effect of the safener isoxadifen-ethyl on the resistance to fenoxaprop-p-ethyl in a biotype of E. crus-galli.RESULTS: A screening of 52 biotypes identified lack of control in the biotype SANTPAT-R treated with the recommended dose of 69 g ha −1 of the commercial formulation of fenoxaprop-p-ethyl with the safener isoxadifen-ethyl. While this biotype survived doses greater than 2208 g ha −1 of the formulation fenoxaprop-p-ethyl + isoxadifen-ethyl, it was killed with 69 g ha −1 of fenoxaprop-p-ethyl without the safener. A glutathione-s-transferase (GST) enzymes inhibitor reduced the resistance factor in two dose-response curves. A minor effect of a CytP450 inhibitor was observed. The previous spraying of the safener isoxadifen-ethyl followed by fenoxaprop-p-ethyl induced survival in the resistant but not in the susceptible biotype. The GST1 and GSTF1 genes were up-regulated in the resistant biotype. ACCase gene mutations were not found, and no cross-resistance to other ACCase inhibitors was identified.CONCLUSION: The safener isoxadifen-ethyl present in the commercial herbicide formulation of fenoxaprop-p-ethyl is associated with resistance in the E. crus-galli SANTPAT-R biotype. This resistance is related with herbicide metabolization mediated by GST pathways. This is the first field-selected weed biotype with herbicide resistance due to safener presence in the sprayed formulation.

Background: Eragrostis plana is an invasive plant in native grassland areas associated with degradation of the Pampa biome. Selective control of E. plana is difficult due to its similarity to other grassland species. There is a lack of information about E. plana control using selective herbicide application equipment. Objective: The present study aimed to evaluate the efficacy of a pressurize rope wick applicator for controlling the invasive plant E. plana as function of different salts of glyphosate, application volumes, and year seasons. Methods: The studies were carried out under field conditions and repeated. The first study evaluated glyphosate salts of isopropylamine, dimethylamine, monoammonium, diammonium, and potassium at doses of 720 and 1440 g ha -1 and clethodim at 60 and 120 g ha -1 . The second study assessed application volumes of 8, 24, 40, and 56 L ha -1 using isopropylamine and potassium salts of glyphosate. Results: Glyphosate applied in summer was more effective at controlling E. plana, with less regrowth than glyphosate application in winter. The glyphosate diammonium was more effective at controlling E. plana than isopropylamine, dimethylamine, monoammonium, or potassium salt formulations at 1440 g ha -1 . Application volume of glyphosate between 8 and 40 L ha -1 provided similar control of E. plana and pasture selectivity. Conclusions: Glyphosate applied with a rope wick selective applicator was effective in controlling E. plana clumps and was selective to grassland. The control efficacy varied as a function of glyphosate salts and year season, but not due to application volume of 8 and 40 L ha -1 .

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In 2015, plants of Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker] were identified in a crop field with an unusual rapid necrosis herbicide symptom after application of 2,4-D. An initial study identified that the symptoms began about 2 h after herbicide application, the resistance factor was high (resistance factor = 19), and the resistance decreased at low light. The mechanism of resistance is not yet known, but the symptomatology suggests it may be related to reduced translocation, ATP-binding cassette (ABC) class B transporters, changes on auxin perception genes, or induction of genes involved in response to pathogens and abiotic stresses. The objective of this study was to use inhibitors of enzymes involved in detoxification and carriers to investigate the mechanisms involved in the resistance to 2,4-D caused by rapid necrosis. Neither the inhibitors of ABC and auxin transporters, triiodobenzoic acid (TIBA), 1-N-naphythylphthalamic acid (NPA), verapamil, and orthovanadate, nor the inhibitors of detoxifying enzymes, such as malathion, 4-chloro-7-nitrobenzofurazan (NBD-Cl), and imidazole, reduced the frequency of the rapid necrosis phenotype. However, orthovanadate and sodium azide (possibly related to auxin transport) were able to partially reduce oxidative stress in leaf disks. The expression of ABCM10 (an ABCD transporter gene), TIR1_1 (an auxin receptor gene), and CAT4 (an amino acid transporter gene) was quickly reduced after 2,4-D application in the resistant accession. Contrary to our hypothesis, LESION SIMULATING DISEASE RESISTANCE 1_3 (LSD1_3) expression increased in response to 2,4-D. LSD1_3 is important for the response to pathogen and abiotic stresses. The rapid necrosis mechanism is not related to 2,4-D detoxification but might be related to changes in the TIR receptor or auxin transport. Mutations in other transporters or in proteins involved in abiotic and pathogen stresses cannot be ruled out.