Abstract

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.

Highlights

  • We previously reported a Palmer amaranth population from Kansas (KSR) with resistance to ALS, PS II, and hydroxyphenylpyruvate dioxygenase- (HPPD-)inhibitor herbicides (Nakka et al, 2017a,b,c)

  • We report for the first time the evolution of six-way resistance in a single Palmer amaranth population, i.e., KCTR with predominance of metabolic resistance mechanisms

  • Our results confirm the evolution of resistance to ALS, PS II, HPPD, PPO, enolpyruvylshikimate-3-phosphate synthase (EPSPS-)inhibitor herbicides, and synthetic auxins in the KCTR population (Table 2)

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Summary

Introduction

Watson) is a topranked troublesome weed in the United States (Van Wychen, 2019) It is a summer annual C4 eudicot species, with a fast growth rate and ability to accumulate biomass (Horak and Loughin, 2000; Sellers et al, 2003). These biological attributes make Palmer amaranth a highly competitive species and if uncontrolled can contribute to drastic yield losses of up to 91% in corn, 79% in soybean, 59% in cotton, and 50% in sorghum (Massinga et al, 2001; Morgan et al, 2001; Bensch et al, 2003; Moore et al, 2004). Resistance to up to five SOAs, i.e., ALS-, EPSPS-, PS II-, HPPD-inhibitor herbicides, and synthetic auxins, was reported in different populations of Palmer amaranth from Kansas (Nakka et al, 2017a,b,c; Kumar et al, 2019; Chaudhari et al, 2020)

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