A nonnative Palmer amaranth (Amaranthus palmeri) population in the Republic of South Africa is resistant to herbicides with different sites of action

Abstract

AbstractPalmer amaranth (Amaranthus palmeriS. Watson) is not native to Africa. Based on the presence and persistence ofA. palmeripopulations, its invasive status in southern Africa is classified as “naturalized.” Globally,A. palmeriis one of the most troublesome weed species in several crops, including soybean [Glycine max(L.) Merr.], maize (Zea maysL.), and cotton (Gossypium hirsutumL.). Certain populations ofA. palmeriin various countries were reported to be resistant to herbicides with different sites of action (SOAs). Two biotypes ofA. palmeriin the United States reportedly each have resistance to herbicides representing five different SOAs, and between them a total of eight different SOAs are involved. Resistance mechanisms in these biotypes involve target-site and/or non–target site resistance. Here we characterize a specificA. palmeripopulation that was found in the Douglas district in South Africa and showed resistance to various herbicide SOAs. Initially, thisA. palmeripopulation was discovered in a glyphosate-tolerant cotton field, where it survived glyphosate treatment. Subsequently, greenhouse experiments were conducted to characterize thisA. palmeripopulation for potential resistance to herbicides of additional SOAs, and molecular analyses were conducted to reveal the mechanisms of herbicide resistance. Results indicated resistance to chlorimuron-ethyl and glyphosate in this population, while <90% control (decreased sensitivity) was observed at the label rate for mesotrione, atrazine, saflufenacil, andS-metolachlor. However, glufosinate, tembotrione, acifluorfen, dicamba, 2,4-D, metribuzin, acetochlor, isoxaflutole, diflufenican, and pyroxasulfone were effective at controlling this population. This profiling of herbicide sensitivity has allowed development of programs to control and potentially minimize the spread of this weed. In addition, molecular analysis ofEPSPSrevealed the role of higher copy number as a mechanism for glyphosate resistance in this population and a Ser-653-Asn target-site mutation likely conferring resistance to the acetolactate synthase–inhibitor chlorimuron-ethyl. No known target-site mutations were identified for the protoporphyrinogen oxidase–inhibitor group.