Lolium rigidum is a ubiquitous weed of cropping systems in southern Australia. It has evolved resistance to numerous herbicides used for its control. Field surveys indicate widespread resistance to post-emergent ACCase- and AHAS-inhibiting herbicides across southern Australia. As a consequence, farming systems now rely on pre-emergent herbicides from just three modes of action for control of this weed in most crops. These are the microtubule elongation inhibitors trifluralin and propyzamide, the lipid synthesis inhibitors triallate and prosulfocarb, and the very long chain fatty acid biosynthesis inhibitors pyroxasulfone and metazachlor. Resistance has evolved to all of these herbicides in recent years. In particular, one population of L. rigidum has been identified that has resistance to all of these herbicides. Susceptible L. rigidum can be protected from triallate and prosulfocarb by P450 inhibitors, but these have no effect on the resistant population. This suggest resistance to these herbicides is the result of a failure to activate these herbicides to their sulfoxide forms. In contrast, P450 inhibitors synergise trifluralin and other pre-emergent herbicides in both susceptible and resistant populations, indicative of P450-based metabolism as the resistance mechanism. Investigations of trifluralin resistance in L. rigidum show that the gene(s) responsible for resistance to trifluralin are different to those responsible for resistance to the post-emergent ACCase-inhibiting herbicides. L. rigidum has the ability to accumulate numerous non-target site resistance mechanisms in addition to target site resistance making long-term control of this weed with herbicides particularly problematic.

What roles for metabolism-based resistance to pre-emergent herbicides in Lolium rigidum

256th National Meeting (2018)

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