Management of glyphosate resistance in summer weeds

Abstract

In Australia, glyphosate resistance continues to evolve in both summer and winter weeds and to date, several mechanisms of glyphosate resistance have been identified. Except for Lolium rigidum, each species appears to have a single mechanism across multiple populations. In the key summer weeds Chloris virgata, Conyza bonariensis, Echinochloa colona and Sonchus oleraceus, resistance appears to be conferred by target-site
mutations.
Amino acid substitutions at Proline106 in the EPSPS enzyme, the target of glyphosate, result in resistance, with different amino acid substitutions giving varying levels of resistance both within and across species. The ploidy level of the species can also affect resistance levels, where the effect of a resistance mutation in EPSPS on one subgenome can be diluted by susceptible forms of the gene on other subgenomes. Conversely, multiple subgenomes allow for the accumulation of two or more resistance mutations, leading to increased levels of resistance.
A series of field trials were established in south-east Queensland to measure the effect of different herbicide strategies and resistance mutations on changes in weed density and population genetics. The four summer species mentioned above were included and there were two or three populations of each species, with different glyphosate resistance mechanisms. Treatments were glyphosate alone and as a double knock, an alternative knockdown of 2,4-D or haloxyfop applied alone or as a double knock, and a residual herbicide treatment of either metolachlor or isoxaflutole.
Over three growing seasons, weed control has differed between treatments and followed the same trend for each weed species with control by residual herbicides > alternative double knock > glyphosate double knock > glyphosate alone. Weed seed samples have been collected over the duration of the trials and will be used to quantify the genetic makeup and shift in weed populations over time.