Biochemical mechanism and inheritance of cross-resistance to acetolactate synthase inhibitors in giant foxtail

Abstract

Giant foxtail putatively resistant to acetolactate synthase (ALS) inhibitors has been reported widely in the upper Midwest, typically in fields with a history of ALS inhibitor use in continuous corn or corn–soybean rotation. However, it is not known whether these giant foxtail populations vary in their response to ALS inhibitors. Therefore, our objectives were to confirm and quantify resistance of giant foxtail accessions from Wisconsin, Minnesota, and Illinois to imidazolinone and sulfonylurea herbicides; to determine the mechanism of resistance; and to determine the mechanism of resistance inheritance. Dose–response experiments using three- to four-leaf stage giant foxtail plants in the greenhouse confirmed cross-resistance of the Wisconsin, Minnesota, and Illinois accessions to imazethapyr and nicosulfuron. Based on ED50 values (the effective dose that reduced shoot dry biomass by 50% compared to the nontreated plants), the Wisconsin, Minnesota, and Illinois accessions were 16-, 17-, and 15-fold resistant to imazethapyr, respectively, and 21-, 19-, and 9-fold resistant to nicosulfuron, respectively, compared to susceptible accessions. In contrast, all accessions were susceptible and responded similarly to fluazifop-P. Based on an in vivo ALS assay, the Wisconsin, Minnesota, and Illinois accessions were > 750-, > 320-, and > 670-fold resistant to imazethapyr, respectively, and 1,900-, > 1,900-, and 80-fold resistant to nicosulfuron, respectively, compared to susceptible accessions. To determine the inheritance of resistance traits, hybrid F1 families were generated from crosses between ALS inhibitor–susceptible and -resistant plants from Minnesota. Three distinct plant phenotypes—resistant (R), intermediate (I), and susceptible (S)—were identified in the F2 generation following exposure to imazethapyr. In repeated experiments, these phenotypes segregated in a 1:2:1 (R:I:S) ratio, indicative of a trait associated with a single, nuclear, semidominant allele.

Green foxtail (Setaria viridis) resistance to acetolactate synthase inhibitors

“…Within the USA, few grass species hâve developed résistance to ALS-inhibiting herbicides, including shattercane {Sorghum bicolor{L.) Moench) (Anderson et al 1998), Italian ryegrass {Lolium multiflorum L.) (Taylor and Coats 1996), wild oat (Avena fatua L.) (Nandula and Messersmith 2000) and giant foxtail (Setaria faberi Herrm.) (Volenberg et al 2001). ALS inhibitor-resistant giant foxtail accessions from Wisconsin, Illinois, and Minnesota are cross-resistant to imidazolinone and sulfonylurea herbicides (Volenberg et al 2001).…”

“…(Volenberg et al 2001). ALS inhibitor-resistant giant foxtail accessions from Wisconsin, Illinois, and Minnesota are cross-resistant to imidazolinone and sulfonylurea herbicides (Volenberg et al 2001).…”

“…Imazethapyr was applied at 0, © 0.70, 1.4, 2.8, 5.6, and 11 g a. Volenberg et al 2000a;Volenberg et al 2001). To obtain dose-response curves, data for each replication were regressed using the following model: ((logl 5 o -logX) b)).…”

Common Cocklebur (<i>Xanthium strumarium</i>) Response to Nicosulfuron

“…This group of herbicides has become popular due to their effectiveness, relatively low use rates, and low mammalian toxicity (Schmidt et al, 2004). Populations of several grass and broad-leaved weed species (Setaria viridis (L.) Beauv., Setaria faberi Herrm., Conyza albida Willd., Amaranthus retroflexus L.) resistant to nicosulfuron have been found (Volenberg et al, 2001;Osuna and De Prado, 2003;Scarabel et al, 2007;Laplante et al, 2009). …”

Control of common cocklebur (Xanthium strumarium L.) with pre- and postemergence herbicides in soybean

“…Three families within Group 2 (sulfonylureas, imidazolinones, and sulfonimides) bind at slightly different sites on the ALS enzyme, potentially allowing plants to be susceptible to some herbicides and resistant to others (Hartzler 1997;Volenberg et al 2001). Most resistant populations have an altered target site on the ALS enzyme, rendering the herbicides ineffective (Volenberg et al 2001). With more options for cocklebur control, there can be a weed management program developed using multiple herbicide groups, which can deter resistance.…”