Palmer amaranth is native to the United States, but was discovered in 2015 in Brazil. Palmer amaranth populations in Brazil were very difficult to control using glyphosate, which resulted in many changes to standard weed management practices. A genotyping assay was used to confirm that the population detected in Mato Grosso State, Brazil, was correctly identified as Palmer amaranth and that it was not tall waterhemp. Greenhouse dose–response curves and shikimate accumulation assays showed that the Brazilian population was highly resistant to glyphosate, with an LD50 value (3,982 g glyphosate ha−1) more than twice the typical use rates and very little shikimate accumulation at 1 mM glyphosate concentrations in a leaf-disk assay. The Brazilian population was also resistant to sulfonylurea and imidazolinone acetolactate synthase (ALS) inhibitor herbicides. The resistance mechanisms in the Brazilian population were identified as increasedEPSPSgene copy number for glyphosate resistance (between 50- and 179-fold relativeEPSPSgene copy number increase) and two different alleles for target-site mutations in theALSgene (W574L and S653N). These results confirm the introduction of Palmer amaranth to Brazil using a genetic marker for species identification, as well as resistance to glyphosate and ALS inhibitors.

Evolution of multiple herbicide resistance in Palmer amaranth across the United States is a serious challenge for its management. Recently, a Palmer amaranth population (KCTR; Kansas Conservation Tillage Resistant) from a long-term conservation tillage research project in Kansas, United States, was found uncontrolled by several commonly used herbicides. Importantly, this field did not have a history of repeated use of some of the herbicides for which the KCTR Palmer amaranth population showed lack of control. The objectives of this study were to confirm the evolution of multiple resistances and determine possible mechanism(s) of resistance in KCTR Palmer amaranth plants. In response to post-emergence application, 28–100% of KCTR Palmer amaranth survived field recommended rates of 2,4-D, ALS-, PS II-, EPSPS-, PPO-, HPPD-inhibitor herbicides, or tank- or pre-mixture of PS II- and HPPD-inhibitor herbicides, confirming evolution of six-way resistance in this Palmer amaranth population. However, this population was found susceptible to the PS I- and glutamine synthetase inhibitor herbicides. Chlorsulfuron-, imazethapyr-, and atrazine-resistant plants did not show any previously reported mutation in ALS and psbA genes, the target sites of these herbicides, respectively. However, the survivors of glyphosate treatment showed amplification of EPSPS gene (up to 88 copies). The KCTR plants pretreated with cytochrome P450 or GST inhibitors along with atrazine, 2,4-D, lactofen, or mesotrione had significantly less biomass accumulation than those treated with herbicides alone. Plants treated with P450 inhibitor followed by imazethapyr showed moderate reduction of biomass in KCTR which was statistically similar to a susceptible Palmer amaranth population treated with imazethapyr. These results suggest predominance of metabolic resistance possibly mediated by cytochrome P450 and GST enzyme activity that may have predisposed the KCTR Palmer amaranth population to evolve resistance to multiple herbicides. This is the first report of evolution of six-way resistance in a single Palmer amaranth population. Appropriate management strategies, including integration of cultural, and mechanical, and herbicide mixtures, are warranted to control such Palmer amaranth populations.

-This work was carried out in order to evaluate the susceptibility to ALS-inhibiting herbicides of the Brazilian biotype of glyphosate-resistant A. palmeri, considering different chemical groups. For that, four experiments were performed, each with one of the following herbicides: glyphosate, chlorimuron-ethyl, cloransulan-methyl and imazethapyr. In each trial, treatments were organized according to a 2x8 factorial scheme, in which two were the species of Amaranthus (A. palmeri and A. spinosus) and eight were the herbicide rates (16D, 8D, 4D, 2D, D, 1/2D, 1/4D and herbicide absence; being D the commercial rate of each product). For glyphosate, D = 720 g a.e. ha ; for imazethapyr, D = 100 g ha -1. Glyphosate was not applied on A. spinosus. In all the trials, the Brazilian biotype of A. palmeri had low herbicide susceptibility, so it was possible to conclude this biotype has ALS-EPSPs multiple resistance. Therefore, considering only ALS-inhibiting herbicides, this population has sulfonilurea-triazolopirimidineimidazolinone cross-resistance. Keywords:Palmer amaranth, dose-response, management, control. Palavras-chave: caruru-palmeri, dose-resposta, manejo, controle. RESUMO -Este trabalho foi desenvolvido com o objetivo de avaliar a suscetibilidade do biótipo brasileiro de

Palmer amaranth (Amaranthus palmeri S. Watson) is a troublesome weed in several cropping systems in the US. The evolution of resistance to multiple herbicides is a challenge for the management of this weed. Recently, we reported metabolic resistance to 2,4-D mediated by cytochrome P450 activity in a 6-way-resistant A. palmeri population (KCTR). Plant growth temperature can influence the herbicide efficacy and level of resistance. The effect of temperature on 2,4-D resistance in A. palmeri is unknown. In this research, we investigated the response of KCTR and a known susceptible (MSS) A. palmeri response to 2,4-D grown at low- (LT, 24/14°C, d/n) or high (HT, 34/24°C, d/n) temperature regimes. When MSS and KCTR plants were 8-10 cm tall, they were treated with 0, 140, 280, 560 (field recommended dose), 1120, and 2,240 g ai ha-1 of 2,4-D. Further, 8-10 cm tall MSS and KCTR plants grown at LT and HT, were also treated with [14C] 2,4-D to assess the metabolism of 2,4-D at LT and HT. The results of dose-response experiments suggest that KCTR A. palmeri exhibits 23 times more resistance to 2,4-D at HT than MSS. Nonetheless, at LT, the resistance to 2,4-D in KCTR was only 2-fold higher than MSS. Importantly, at HT there was enhanced metabolism of 2,4-D in both KCTR and MSS A. palmeri, than at LT. Further, treatment with cytochrome P450- inhibitor, malathion followed by 2,4-D increased the susceptibility of KCTR at HT. Overall, rapid metabolism of 2,4-D increased KCTR resistance to 2,4-D at HT compared to LT. Therefore, the application of 2,4-D when temperatures are cooler can improve control of 2,4-D-resistant A. palmeri.

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