The response of ACCase-resistant Phalaris paradoxa populations involves two different target site mutations

Phalaris paradoxa (awned canary-grass) is an aggressive annual winter weed in wheat and other arable crops that is controlled mainly by ACCase-inhibiting herbicides: cyclohexanediones (DIMs), aryloxyphenoxypropionates (FOPs) and phenylpyrazolines (DENs, e.g. pinoxaden). The selection pressure imposed on the weed populations by repeated use of these herbicides has resulted in the evolution of increased numbers of ACCase-resistant populations of P. paradoxa in Israel and other countries. Two populations, Revadim (RV) and Mishmar Ha'emek (MH) that were exposed to differing weed and crop management tactics were investigated. Both populations were highly resistant to all FOPs, pinoxaden and cycloxydim, but responded differently to some DIMs. RV plants exhibited much higher resistance to tralkoxydim than MH plants, while showing similar low levels of resistance to tepraloxydim and clethodim. Both populations were equally susceptible to graminicides with other modes of action. The mutations responsible for the observed resistance were identified using PCR-RFLP and by sequencing the carboxyl transferase domain of the chloroplastic ACCase gene. RV plants possess a substitution of Asp₂₀₇₈ to Gly, whereas in MH population a mixture of Ile₂₀₄₁ to Asn or Asp₂₀₇₈ to Gly was found. Our study demonstrates that lack of herbicide and crop rotation may result in the evolution of diverse target site mutations and differential response of the whole plant to ACCase inhibitors.     

Allelic variation of the ACCase gene and response to ACCase-inhibiting herbicides in pinoxaden-resistant Lolium spp

BACKGROUND: The repeated use of acetyl‐coenzyme A carboxylase (ACCase) inhibiting herbicides to control grass weeds has selected for resistance in Lolium spp. populations in Italy. The efficacy of pinoxaden, a recently marketed phenylpyrazoline herbicide, is of concern where resistance to ACCase inhibitors has already been ascertained. ACCase mutations associated with pinoxaden resistance were investigated, and the cross‐resistance pattern to clodinafop, haloxyfop, sethoxydim, clethodim and pinoxaden was established on homo/heterozygous plants for four mutant ACCase alleles. RESULTS: Seven different mutant ACCase alleles (1781‐Leu, 1999‐Leu, 2041‐Asn, 2041‐Val, 2078‐Gly, 2088‐Arg and 2096‐Ala) and 13 combinations with two types of mutation were detected in the pinoxaden‐resistant plants. The 1781‐Leu allele appears to confer a dominant resistance to pinoxaden, clodinafop, haloxyfop, sethoxydim and clethodim at 60 g AI ha^?1. The 2041‐Asn and 2041‐Val alleles are associated with dominant or partially dominant resistance to FOPs, no substantial resistance to DIMs and a moderate resistance to pinoxaden. The 2088‐Arg allele endows a partially dominant resistance to clodinafop, sethoxydim and most likely to pinoxaden. In addition, non‐target‐site resistance mechanisms seem to be involved in pinoxaden resistance. CONCLUSION: Almost all the ACCase mutations selected in the field by other ACCase inhibitors are likely to confer resistance to pinoxaden. Although pinoxaden is sometimes able to control FOP‐resistant populations, it should not be considered as a sustainable ACCase resistance management tool. The presence of non‐ACCase‐based resistance mechanisms that could confer resistance to herbicides with different modes of action further complicates the resistance management strategies. Copyright © 2011 Society of Chemical Industry