Pinoxaden resistance in Lolium perenne L. is due to both target-site and non-target-site mechanisms

Application of herbicides inhibiting acetyl CoA carboxylase (ACCase) has been one of the main strategies for selectively controlling grass weed species such as perennial ryegrass (Lolium perenne L.) in wheat and barley crops in New Zealand. In this study, we have confirmed and characterized resistance to pinoxaden, an ACCase-inhibiting herbicide, in a population of L. perenne. Dose-response experiments were conducted to assess the level of pinoxaden resistance, and based on the LD50 values, the studied population was 41.4-times more resistant to pinoxaden than a susceptible population. Application of malathion, an inhibitor of the cytochrome P450s, preceding pinoxaden treatment reduced the level of resistance to 9.7-fold. However, pre-treatment with the glutathione S-transferase (GST) inhibitor 4-chloro7- nitrobenzoxadiazole prior to pinoxaden treatment did not affect pinoxaden resistance. Partial sequencing of the ACCase gene revealed that the resistant population had an isoleucine to valine replacement at position 2041. These results suggest that both cytochrome P450-based and target-site mechanisms are jointly associated with this instance of pinoxaden resistance in L. perenne. The pinoxaden-resistant L. perenne individuals were also resistant to quizalofop-p-ethyl (108.6-fold), but they were susceptible to clethodim, which can, therefore, be used to manage this pinoxaden-resistant L. perenne. This is the first report of a L. perenne population in which a rare target-site mutation works in concert with enhanced cytochrome P-450 activity to confer pinoxaden resistance. Evolution of resistance to ACCase-inhibiting herbicides in this L. perenne population indicates that integrated weed management practices are required to prevent widespread resistance developing in New Zealand cereal crop systems.

Automated summary

Resistance to ACCase-inhibiting herbicide pinoxaden in a population of L. perenne is characterized by the concurrent action of cytochrome P-450 activity enhancement and a rare target-site mutation. The resistant population showed different levels of resistance to other herbicides but remained susceptible to clethodim.